ISAAC_OCHIENGS_REVISION_SERIES_ANSWERS_TO_THE_ASSORTED_VIROLOGY

ISAAC OCHIENG’S REVISION SERIES
ANSWERS TO THE ASSORTED VIROLOGY SAQS FOR MBCHB/BDS

(ADAPTED FROM DEPARTMENTAL PAST PAPERS)
PREAMBLE: LESSONS LEARNT FROM THE LATE DR. ISAAC OCHIENG
Inspired by the zeal and passion Isaac exuded, our prayer is that we may emulate the same and
by God’s grace may this help transform the approach to and perception of our academics.
Through this, may we neither be found stagnant in the maze of reading for the sake of exams,
nor in that of getting just enough to make the cut to the next year. May the lessons we learnt
from Isaac in his livelihood and even more as he rests, transform our experience in med school,
snuff out the mediocrity that we most at times find ourselves entrapped in. May in our lives be
ignited the joy, passion, zeal, and even more the irresistible urge to study Medicine for the love
and sake of Medicine. Beyond this, may we seek to explore all available opportunities, expend all
available resources, considerably use our time, obey the tutelage of our predecessors and give
ourselves fully to all that shall rightfully contribute towards molding us into exquisite and well-
equipped practitioners on all fronts. Deep down, may our desire always be to make a difference,
to revolutionize the practice of medicine, all for the glory and honor of God! But even in all
these, may God be our light, our standard and the image from whom we reflect, seek to become
and get guidance from, lest we lose our way. For God alone can guarantee our safe voyage in the
path towards becoming the great practitioners He has fashioned us forth to become. Baraka!
VINCENT, SAMARA, EFFIE, MULKI, FIONA & DUBAT. TO THE GLORY AND HONOUR OF GOD! 1
“WHERE GOD LEADS, HE PROVIDES. WHERE HE GUIDES, HIS

GRACE IS SUFFICIENT”
1. OUTLINE THE CLASSES AND MECHANISM OF ACTION OF ANTI-
RETROVIRAL AGENTS (ARV)
Receptor binding inhibitors:
• Maraviroc: Blocks CCR5 co-receptor preventing binding of HIV
Fusion inhibitors:
• Enfurvitide- Binds HIV- gp41 hence preventing fusion with host cell
membrane
• Palivizumab- Monoclonal antibody that binds F protein of Respiratory
Syncytial Virus (RSV) preventing fusion
Agents that block uncoating:
• Amantadine/ Rimantadine- Block M2 ion channels – a viral protein. Prevents
acidification of the endosome which is required for uncoating. Active on
Influenza A only.
• Resistance is widespread especially in H1N1 and H3N2 strains
Nucleic acid synthesis inhibitors:
a) DNA synthesis inhibitors
DNA polymerase inhibitors- Incorporated into DNA chain by DNA polymerase
causing termination. Nucleoside analogues- Acyclovir and Idoxyuridine
i. Acyclovir is a prodrug active against HSV-1 HSV-2 and VSV. It undergoes
three phosphorylation steps to become active. The first step is by viral
Thymidine kinase while the subsequent steps are done by the host cell enzymes.
The triphosphate form then is incorporated into the viral genome causing chain
termination.
ii. Idoxyuridine is a pyrimidine analogue that inhibits DNA polymerase. Its toxic
effect is due to its non-selectivity hence it can also inhibit human DNA
polymerase. It has been replaced by Acyclovir.
Reverse transcriptase inhibitors- Block DNA synthesis from RNA by inhibiting the
function of the enzyme RNA transcriptase (RNA dependent DNA polymerase)
• -Nucleoside Reverse Transcriptase Inhibitors (NRTIs)- Zidovudine
Lamivudine, Abacavir
• -Nucleotide Reverse Transcriptase Inhibitors (NtRTIs)- Tenofovir
• Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs)- Nevirapine,
Efavirenz Etravirine
b) DNA Integrase Inhibitors- Prevent integration of DNA into the host genome by
binding to the integrase enzyme. All are ARVs – Raltegravir Dolutegravir
Elvitegravir
c) RNA Synthesis Inhibitors- Block the action of RNA polymerase.
• Ribavirin- Inhibits the RNA polymerase of RNA viruses such as Hepatitis C

(HCV) and Influenza. It prevents capping of mRNA in Influenza virus
Safosbavir- Inhibits Hepatitis C RNA polymerase.
d) Novel RNA synthesis inhibitor-
• Favipiravir. Inhibits RNA polymerase in several viruses like Influenza. It has
in-vitro activity against Arenaviridae, Bunyaviridae, Flaviviridae and others.
Protein Synthesis Inhibitors-
• Formivirsen: It is an anti-sense oligonucleotide that binds complementary to
RNA of Cytomegalovirus (CMV). It prevents the translation of mRNA into
protein. It is used to treat CMV Retinitis.
• Protease Inhibitors- They bind protease preventing protein cleavage hence
blocking viral maturation.
• Hepatitis C – Simeprevir Paritaprevir
• HIV- Lopinavir Ritonavir
Viral Release Inhibitor-
Oseltamivir/ Zanamivir: They block viral neuraminidase of Influenza A and B. Sialic
acid is the influenza virus receptor. Neuraminidase clears sialic acid from the infected
cell surface and respiratory mucus secretions. This allows the Influenza virus to spread
to uninfected cells.
Interferons:
Are cytokines with antiviral, immunomodulatory and anti-proliferative activity. Bind
specific cellular receptors to induce genetic expression through the JAK-STAT
pathway leading to synthesis of several proteins which have antiviral activity through
inhibition of: Transcription, Translation, Post-translational modification of protein,
Virus maturation Virus release. They are used in Hepatitis B and C infections. They
include Natural INF, Recombinant INF, Pegylated INF.
2. DESCRIBE ANTIGENIC VARIATION AS REGARDS TO INFLUENZA
VIRUSES.
Influenza strains are constantly mutating. Small changes to the genetic makeup of
influenza strains are referred to as antigenic drift, while a major change is called
antigenic shift. When the flu strain mutates, our immune system recognizes it as a new
virus. The antibodies created in response to having the flu in the past are unable to
protect against the new strain. These genetic mutations are why we can contract the flu
more than once, and the reason the influenza vaccine is changed annually and may be
less effective in some flu seasons than others.
Antigenic Drift:
A minor change to the flu virus is known as antigenic drift. Both influenza A and B
viruses undergo antigenic drift. These mutations in the virus’s genes can lead to
changes in its surface proteins hemagglutinin (HA) and neuraminidase (NA).
These proteins, known as antigens, are recognized by the immune system, prompting
an immunological response that can result in illness and promote immunity in the
future. As the virus replicates, these changes in antigenic drift happen continually. Over
time, these small changes accumulate and result in a new strain that is not recognized
by the immune system. This antigenic drift is the reason we need new flu vaccines
every year and the reason we can get sick from the flu multiple times in our lives.
Antigenic Shift: Antigenic shift is a more major change in the influenza virus. This shift typically
occurs when a human flu virus crosses with a flu virus that usually affects animals (such as birds
or pigs). When the viruses mutate, they shift to create a new subtype that is different from any seen
in humans before. This can happen in three ways:
1. A human flu virus infects an animal such as a pig. The same pig also gets infected by a flu
virus from another animal such as a duck. The two flu viruses can mix and mutate, creating
a completely new type of flu virus that can then spread to humans.
2. A strain of bird flu passes to humans without undergoing any type of genetic change.
3. A strain of bird flu passes to another type of animal (such as a pig) and is then passed on
to humans without undergoing a genetic change.
When a major antigenic shift like this occurs, very few people have any type of immunity to the
new, or "novel," flu virus. When flu pandemics have occurred in recent known history, it has been
due to an antigenic shift in the virus. Fortunately, these shifts occur only occasionally, having
caused only four true flu pandemics in the past century.
This major antigenic shift only happens to influenza A viruses, not in influenza B viruses
(they only undergo antigenic drift).
3. DESCRIBE BRIEFLY THE ADVANTAGES AND DISADVANTAGES OF

INACTIVATED VACCINE.
Inactivated vaccine is derived from disease causing pathogens (viruses or bacteria) that
have been killed through physical or chemical process however their antigens are
preserved and hence cannot revert to cause disease but can help confer immunity.
Examples are the Inactivated Polio Virus and Whole cell Pertussis.
Advantages
• Have no live components as risk of inducing the disease hence considered safer
and more stable.
Disadvantages
• It may not always induce an immune response at first dose.
• Response may be long lived hence requiring several doses of the vaccine.
B. WRITE BRIEF NOTES ON LIVE ATTENUATED VACCINES
Viruses may be attenuated via passage of the virus through a foreign host, such as:
1. Tissue culture
2. Embryonated eggs
3. Live animals
The initial virus population is applied to a foreign host. One or more of these will
possess a mutation that enables it to infect the new host. These mutations will
spread, as the mutations allow the virus to grow well in the new host; the result is
a population that is significantly different from the initial population, and thus
won’t grow well in the original host when it's reintroduced (hence is 'attenuated').
This process is known as "passage" in which the virus becomes so well adapted to
the foreign host that it is no longer harmful to the vaccinated subject. This makes it
easier for the host's immune system to eliminate the agent and create the
immunological memory cells which will likely protect the patient if they are
infected with a similar version of the virus in "the wild".
4. OUTLINE 5 DIFFERENCES BETWEEN HEPATITIS A AND C VIRUS

Variable Hepatitis A Hepatitis C

Family Picornaviridae Flaviviridae
Transmission Feco-oral Blood/body fluids
Chronic infection No Yes (70% of cases)
Vaccine Yes No
Antivirals No Yes
5. LIST 5 CAUSES OF VIRAL GASTROENTERITIS
• Poliovirus
• Coxsackie A and B virus
• Enteroviruses 68-71 virus
• Hepatitis A virus.
• Hepatitis E virus.
• Adenoviruses 1-39 viruses
• Reoviruses.
6. WRITE BRIEF NOTES OF ON LABORATORY DIAGNOSIS OF VIRAL
INFECTIONS UNDER THE FOLLOWING TOPICS:
a. ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA)
ELISA is an example of a serology test. There are two types, antibody ELISA
and antigen ELISA. For an antibody ELISA, antigens are stuck onto a plastic
surface, a sample is added and any antibodies for the disease we are testing for
will bind to the antigens. Next a second antibody with a marker is added and a
positive reaction is detected by the marker changing color when an appropriate
substrate is added. If there are no antibodies in the sample, the second antibody
will not be able to stick and there will be no color change. For an antigen
ELISA, antibodies are bound to a plastic surface, a sample is added and if
antigens from the virus we are testing for are present they will stick to the
antibodies. This test then proceeds in the same way as the antibody ELISA. If
properly performed, these tests have a sensitivity and specificity exceeding
98%. When ELISA-based antibody tests are used for screening populations
with a low prevalence of HIV infections (eg, blood donors), a positive test in a
serum sample must be confirmed by a repeat test. If the repeat EIA test is
reactive, a confirmation test is performed to rule out false-positive ELISA
results.
b. IMMUNOFLUORESCENCE ASSAY (IFA)
Immunofluorescence assay (IFA) is a standard virologic technique used to
identify the presence of antibodies by their specific ability to react with viral
antigens expressed in infected cells; bound antibodies are visualized by
incubation with fluorescently labelled antihuman antibody.
7. WRITE BRIEF NOTES ON PRIONS UNDER THE FOLLOWING HEADINGS:
a. DEFINE PRIONS
They are small proteinaceous Infectious particles that are resistant to

inactivation by procedures that usually modify/denature proteins.
b. DESCRIBE HOW THEY CAUSE DISEASES
KEY FEATURE: Accumulation of abnormal prion protein PrPsc
• Normal cellular protein (PrPc) is found on the surface of brain cells & other
cells
• Infection or Mutation of PRNPgene on c.20 can cause PrPc to misfold into
PrPsc
• PrPsc dissociates from the cell membrane
• PrPsc causes more PrPc to misfold and dissociate from the cell surface
• Accumulation of PrPsc forms proteinaceous plaques between the brain cells
• Aggregated PrPsc is then internalized into cells >>spongiform appearance
8. WRITE BRIEF NOTES ON THE FOLLOWING:

a. MECHANISM BEHIND HUMAN PAPILLOMA VIRUS CAUSATION
OF CERVICAL CANCER
HPV invades the skin or mucosa by entering tiny breaks in the surface (even
those not visible to the naked eye). Once inside, HPV infects host epithelial
cells, tricking them into producing new viruses. In the process of normal cell
replacement, the infected cells are shed, releasing viral particles. High risk
strains of HPV can integrate viral DNA into the host genome, although this is
not a normal part of the HPV life cycle. Viral integration may give infected host
cells a selective advantage, leading to a longer infection time. The longer the
infection lasts, the more time there is for cancer to develop. After integration,
two viral genes (E6 and E7) may be over-expressed. The E6 and E7 proteins
are responsible for the ability of HPV to cause cancer. The E6 and E7 proteins
prevent the activity of key tumor suppressors. E6 inhibits p53, a protein that
controls responses to different types of cellular stress including DNA damage
and viral infection. E7 inhibits Rb, a protein that can prevent cell division by
blocking the activity of transcription factors. The combined effects of E6 and
E7 put cells at risk for undergoing uncontrolled division that can lead to cancer.
The HPV genome contains several genes that encode proteins. In HPV, three of
these genes, E2, E6, and E7, are of particular interest because of their roles in
the development of cervical cancer. The E2 protein functions by binding to both
the E6 and E7 proteins. When E6 and E7 are bound to E2 they are blocked from
acting in the cell. When E6 is not bound to E2, it is free to bind to the p53 tumor
suppressor. When E6 binds to p53, p53 is destroyed and cannot function. p53
is a key protein in cell cycle control. It is not functional in over 50% of all
human cancers. Without the p53 protein, a cell may continue to divide even if
it is damaged. The E6 protein also causes the expression of telomerase.
Telomerase is a protein that is not normally produced by most cells in adult
humans. When it is present, telomerase maintains the ends of the chromosomes.
This prevents the breakdown of chromosomes and helps cancer cells to divide
forever. Another HPV protein, E7, also plays a key role in helping the virus
take over control of infected cells. When not bound by E2, E7 binds to another
protein, Rb. When E7 is bound to Rb, Rb cannot carry out its normal function.
Normally, Rb binds to E2F. E2F is a transcription factor that causes cell cycle
progression. When E2F is bound to Rb, it cannot act as a transcription factor
and cannot cause the cell to divide. But, if E7 binds to Rb, E2F cannot also bind
to Rb and is then free to act as a transcription factor. In essence, E7 inhibits an
inhibitor or cell division. When a cell makes the E7 protein, the E2F
transcription factor causes the cell to divide, a critical step in cancer
development. The E6 and E7 proteins help HPV hijack cell division and help
drive cancer development.
b. COMPLICATIONS ASSOCIATED WITH HUMAN PAPILLOMA
VIRUS IN THE 1ST 20 WEEKS OF PREGNANCY
HPV can replicate in trophoblasts leading to (1) inhibition of blastocyst
formation; (2) failed or suboptimal endometrial implantation of trophoblastic
cells; and (3) apoptosis of embryonic cells. Besides these direct effects on
placenta cells, it has been hypothesized that HPV-trophoblast interaction may
trigger immune hypersensitivity to bacteria leading to pregnancy
complications, such as:
• Preterm rupture of membranes
• Preeclampsia
• Fetal growth restriction
• Preterm delivery
• Placental abnormalities
c. HUMAN PAPILLOMA VIRUS THERAPEUTICS
In most immunocompetent people, warts are a cosmetic nuisance and will
eventually disappear spontaneously. Warts may be destroyed by cryotherapy
with dry ice or liquid nitrogen, but simple topical treatment with salicylic acid
at home is often successful. Interferon, photodynamic therapy and indole-3-
carbinol have been used for treatment of recurrent laryngeal warts after the
reduction of tumor load by cautery or excision. Genital warts are more
problematic. Many treatments can be used for genital warts including:
• Antiproliferative agents such as podophyllin or 5-fluorouracil,
although close monitoring is required
• Destructive therapies such as trichloracetic acid, liquid nitrogen or
surgical excision
• Immunomodulators such as imiquimod, which activates
monocytes/macrophages and causes direct release of interferon-α
(self-applied topical treatment).
All of these treatments will remove the lesions but do not always eradicate the
virus from surrounding normal epithelium.
9. LIST 5 CLASSES OF ANTI-VIRAL AGENTS OTHER THAN ARVS, GIVING

AN EXAMPLE OF A DRUG IN EACH CASE AND THE DISEASE IT IS USED
IN.
10. WRITE SHORT ESSAYS ON THE FOLLOWING:

a. PATHOGENESIS OF POLIOVIRUS
The mouth is the portal of entry of the virus, and primary multiplication takes
place in the oropharynx or intestine. The virus is regularly present in the throat
and in the stools before the onset of illness. One week after infection, there is
little virus in the throat, but virus continues to be excreted in the stools for
several weeks even though high antibody levels are present in the blood. The
virus may be found in the blood of patients with nonparalytic poliomyelitis.
Antibodies to the virus appear early in the disease, usually before paralysis
occurs. It is believed that the virus first multiplies in the tonsils, the lymph nodes
of the neck, Peyer patches, and the small intestine. The CNS may then be
invaded by way of the circulating blood. Poliovirus can spread along axons of
peripheral nerves to the CNS, where it continues to progress along the fibers of
the lower motor neurons to increasingly involve the spinal cord or the brain.
Poliovirus invades certain types of nerve cells, and in the process of its
intracellular multiplication, it may damage or completely destroy these cells.
Poliovirus does not multiply in muscle in vivo. The changes that occur in
peripheral nerves and voluntary muscles are secondary to the destruction of
nerve cells. Some cells that lose their function may recover completely.
Inflammation occurs secondary to the attack on the nerve cells. In addition to
pathologic changes in the nervous system, there may be myocarditis, lymphatic
hyperplasia, and ulceration of Peyer patches.
b. INSERTIONAL MUTAGENESIS IN RELATION TO VIRUSES
Insertional mutagenesis is the creation of mutations of DNA by addition of one
or more base pairs. Such insertional mutations can occur naturally, mediated by
viruses or transposons, or can be artificially created for research purposes in the
lab.
Even though many viruses integrate their own genomes into the genomes of
their host cells in order to replicate, insertional mutagenesis caused by viral
infections is not caused by all integrating viruses.
Some DNA insertions will lead to no noticeable mutation. The lentiviral vectors
used to insert therapeutic DNA showed no tendency to disrupt gene function or
promote oncogenic development hence it is now considered safe to use such
integrating vectors for gene therapy. An advantage is that the lentiviral vectors
integrate the DNA permanently, whereas other, non-integrating, viruses' effect
is transient. For those viruses such as gamma retroviruses that tend to integrate
their DNA in genetically unfavorable locations, the severity of any ensuing
mutation depends entirely on the location within the host's genome wherein the
viral DNA is inserted. If the DNA is inserted into the middle of an essential
gene, the effects on the cell will be drastic. Additionally, insertion into a gene's
promoter region can have equally drastic effects. Likewise, if the viral DNA is
inserted into a repressor, the promoter's corresponding gene may be over-
expressed – leading to an overabundance of its product and altered cellular
activity. If the DNA is inserted into a gene's enhancer region, the gene may be
under-expressed – leading to relative absence of its product, which can
significantly interrupt the activity of the cell.
Alteration of different genes will have varying effects on the cell. Not all
mutations will significantly affect the proliferation of the cell. However, if the
insertion occurs in an essential gene or a gene that is involved in cellular
replication or programmed cell death, the insertion may compromise the
viability of the cell or even cause the cell to replicate interminably – leading to
the formation of a tumor, which may become cancerous.
Insertional mutagenesis is possible whether the virus is of the self-inactivating
types commonly used in gene therapy or competent to replicate. The virus
inserts a viral oncogene normally near the cellular myc (c-myc) gene. The c-
myc gene is normally turned off in the cell; however, when it is turned on it is
able to push the cell into the G1 phase of the cell cycle and cause the cell to
begin replication, causing unchecked cell proliferation while allowing the viral
gene to be replicated. After many replications where the viral gene stays latent
tumors begin to grow. These tumors are normally derived from one
mutated/transformed cell (clonal in origin). Avian leukosis virus is an example
of a virus that causes a disease by insertional mutagenesis. Newly hatched
chicks infected with Avian leukosis virus will begin to form tumors that will
begin to appear in their bursa of fabricius (like the human thymus). This viral
gene insertion is also known as a promoter insertion as it drives the expression
of the c-myc gene. There is an example of an insertional mutagenesis event
caused by a retrotransposon in the human genome where it causes Fukuyama-
type muscular dystrophy.
11. WRITE SHORT NOTES ON THE MECHANISMS OF HIV-1 LATENCY
An immune response to HIV occurs 1 week to 3 months after infection, plasma viremia
drops, and levels of CD4 cells rebound. However, the immune response is unable to
clear the infection completely, and HIV-infected cells persist in the lymph nodes. This
period of clinical latency may last for as long as 10 years. During this time, there is a
high level of ongoing viral replication. It is estimated that 10 billion HIV particles are
produced and destroyed each day.
12. BRIEFLY DEFINE THE FOLLOWING TERMS:
a. VACCINE: a substance used to stimulate the production of antibodies and
provide immunity against one or several diseases, prepared from the causative
agent of a disease, its products, or a synthetic substitute, treated to act as an
antigen without inducing the disease.
A vaccine are microbes that are dead or inactive (unable to cause disease)
introduced into the body to stimulate the body’s immune response. It is given
to prevent an infectious disease from developing and the person becoming ill.
b. LATENCY: the state or period of living or developing in a host without
producing symptoms
Latency is a type of persistence whereby the virus is present in the form of its
genome only and there is limited expression of viral genes.
c. HAPTEN: a small molecule which, when combined with a larger carrier such
as a protein, can elicit the production of antibodies which bind specifically to it
(in the free or combined state)
Hapten is a molecule that reacts with specific antibody but is not immunogenic
by itself, it can be made immunogenic by conjugation to a suitable carrier.
d. ANTIGEN: a toxin or other foreign substance which induces an immune
response in the body, especially the production of antibodies
e. ANTIBODY: a blood protein produced in response to and counteracting a
specific antigen. Antibodies combine chemically with substances which the
body recognizes as alien, such as bacteria, viruses, and foreign substances in
the blood
An antibody (Ab), also known as an immunoglobulin (Ig), is a large protein
produced by B-cells that is used by the immune system to identify and
neutralize foreign objects, such as bacteria and viruses.
13. BRIEFLY DISCUSS THE FOLLOWING:
a. CLINICAL PRESENTATION DUE TO ACUTE VIRAL HEPATITIS
• Fever (37.5- 39.0)
• Jaundice
• Pain/tenderness in the upper abdomen
• Dar colored urine
• Pale colored stool
b. RISK FACTORS ASSOCIATED WITH HIV ACQUISITION OR
INFECTION
• The presence of other sexually transmitted diseases such as syphilis,
gonorrhea, or herpes simplex type increases the risk of sexual HIV
transmission as much as a 100-fold because the inflammation and sores

facilitate the transfer of HIV across mucosal barriers.
• Some routes of transmission have higher risk of HIV transmission than
others (intravenous> Rectal > Vaginal). Blood transfusion – 93%,
Receptive anal sex – 1.4%, Insertive anal sex – 0.1%, Receptive Vaginal
Sex – 0.08%, Insertive vaginal sex – 0.04%, Oral sex – very low
• Some genotypes are more infective than others. HIV -1 is easily transmitted
compared to HIV – 2
• Host susceptibility to infection. The host may lack CD4 receptors
preventing the virus from infecting the host cell.
Behaviors and conditions that put individuals at greater risk of contracting HIV
include:
• Having unprotected anal or vaginal sex;
• Having another sexually transmitted infection (STI) such as syphilis,
herpes, chlamydia, gonorrhea and bacterial vaginosis;
• Sharing contaminated needles, syringes and other injecting equipment and
drug solutions when injecting drugs;
• Receiving unsafe injections, blood transfusions and tissue transplantation,
and medical procedures that involve unsterile cutting or piercing; and
• Experiencing accidental needle stick injuries, including among health
worker
c. PASSIVE IMMUNIZATION AGAINST VIRAL DISEASE
Artificial passive immunization is used in clinical practice when it is considered
necessary to protect a patient at short notice and for a limited period.
Antibodies, which are antiviral, in preparations of human or animal serum are
injected to give temporary protection. Human preparations are referred to as
homologous, and are much less likely to give rise to the adverse reactions
occasionally associated with the injection of animal (heterologous) sera. An
advantage of homologous antisera is that, although they do not confer durable
protection, their effect may persist for 3–6 months. Preparations of specific
immunoglobulins are available for passive immunization against the following:
• Tetanus (human tetanus immunoglobulin; HTIG)
• Hepatitis B (HBIG)
• Rabies (HRIG)
• Varicella–zoster (ZIG).
d. PATHOGENESIS OF ROTAVIRUS
• Enterocytes at villous tips are initially infected; the virus binds surface
carbohydrates and penetrates the cell membrane leading to transcription of
viral RNA
• Damage to the mucosa leads to malabsorption
• Activity of disaccharidases and peptidases in the brush border is decreased
and osmosis from unabsorbed nutrients contributes to the diarrhea
• Glucose cotransport of electrolytes is decreased but oral rehydration

solutions are still affective
• Mature enterocytes are lost and initially replaced by immature secretory
cells
• There is net secretion of water in part mediated by the enteric nervous
system
• Clearance of infection is complex and involves overlapping elements of
innate, cellular and humoral immunity
• Virus is usually shed for 6 to 10 days after patients become symptomatic
In summary:
Rotaviruses infect cells in the villi of the small intestine (gastric and colonic
mucosa are spared). They multiply in the cytoplasm of enterocytes and
damage their transport mechanisms. One of the rotavirus encoded proteins,
NSP4, is a viral enterotoxin and induces secretion by triggering a signal
transduction pathway. Damaged cells may slough into the lumen of the
intestine and release large quantities of virus, which appear in the stool (up
to 1012 particles per gram of faeces). Viral excretion usually lasts from 2 to
12 days in otherwise healthy patients but may be prolonged in those with
poor nutrition. Diarrhea caused by rotaviruses may be due to impaired
sodium and glucose absorption as damaged cells on villi are replaced by
non-absorbing immature crypt cells. It may take from 3 to 8 weeks for
normal function to be restored.
e. YELLOW FEVER VIRUS
• Yellow fever virus is the member of the Flaviviridae family.
• It causes yellow fever, an acute, febrile, mosquito borne illness that occurs
in the tropics and subtropics of Africa and South America).
• The virus is introduced by a mosquito through the skin, where it multiplies.
It spreads to the local lymph nodes, liver, spleen, kidney, bone marrow, and
myocardium. It is present in the blood early during infection.
• The lesions of yellow fever are caused by the localization and propagation
of the virus in a particular organ. The incubation period is 3–6 days.
• Symptoms are fever, chills, headache, dizziness, myalgia, and backache
followed by nausea, vomiting, and bradycardia. The disease can progress to
a more severe form, with fever, jaundice, renal failure, and hemorrhagic
manifestations.
• Laboratory diagnostic techniques are Virus Detection or Isolation and
Serology.
• There is no anti-viral drug therapy. Only the symptoms are treated.
Vaccines are available to prevent people from getting infected
14. LIST THE VIRAL CAUSES OF SEXUALLY TRANSMITTED DISEASES
STIs caused by viruses include:
• Hepatitis B,
• Herpes
• HIV
• Human papilloma virus (HPV).
a.OUTLINE THE STRUCTURE, EPIDEMIOLOGY AND
COMPLICATIONS ASSOCIATED WITH ONE OF THE VIRUSES
YOU’VE LISTED ABOVE
a. MECHANISM OF ACTION OF ACYCLOVIR
Acyclovir is converted to its triphosphate form, acyclovir triphosphate (ACV-
TP), which competitively inhibits viral DNA polymerase, incorporates into and
terminates the growing viral DNA chain, and inactivates the viral DNA
polymerase. It is a prodrug active against HSV-1 HSV-2 and VSV. It undergoes
three phosphorylation steps to become active. The first step is by viral
Thymidine kinase while the subsequent steps are done by the host cell enzymes.
The triphosphate form then is incorporated into the viral genome causing chain
termination.
b. CLASSES OF DRUGS USED TO TREAT HIV-AIDS PATIENTS
• Reverse Transcriptase Inhibitors – These inhibit the action of the enzyme
reverse transcriptase blocking the synthesis of DNA from RNA. There are
two inhibitors:
• Nucleoside & Nucleotide Reverse Transcriptase Inhibitors (NRTIs):
Examples are Zidovudine, Lamivudine, Abacavir, Tenofovir
• Non-Nucleoside RT Inhibitors: Examples are Nevirapine, Efavirenz,
Etravirine
• Protease Inhibitors: These bind to the enzyme protease. This prevents
protein cleavage hence blocks viral maturation. Examples are Ritonavir,
Lopinavir, Atazanavir, Darunavir
• Integrase inhibitors: These binds to the enzyme integrase hence
preventing integration of HIV into host DNA. Examples are Raltegravir,
Dolutegravir
• Fusion inhibitors: These interfere with the binding & fusion of HIV with
cell membrane. An example is Enfuvirtide
• CCR5 antagonists (against R5-tropic viruses): These bind to the CCR5
co-receptor preventing attachment of the virus. An example is Maraviroc
c. CHRONIC HEPATITIS INFECTION
Background: Chronic infection can only occur in HBV, HCV & HDV. HBV-
HIV co-infections have higher rates if chronicity of hepatitis
i. HBV
Epidemiology: 5% of global population (400 million) have chronic HBV
infection. 90% of infected infants develop chronic infection, Approx. 5% of
adults develop chronic infection
Possible outcomes of Chronic HBV infection:
• Asymptomatic Chronic Infection (carrier)

• Chronic Persistent Hepatitis
• Chronic Active Hepatitis
• Cirrhosis
• Hepatocellular Carcinoma
Chronic HBV symptoms:
• Malaise, fatigue, weakness
• Weight loss
• Peripheral edema
• Ascites
• Extra-hepatic manifestations
Chronic HBV Complications (Extra-hepatic manifestations):
• Resp: Pleural effusions/ hepatopulmonary syndrome
• CVS: arrhythmias, pericarditis, myocarditis, arteritis
• CNS: encephalopathy, somnolence, confusion
• Muscoskeletal system: arthralgia, Serum sickness
• Renal: Glomerulonephritis,
• Hematological: bone marrow aplasia
Lab diagnosis (Serology):
HBsAG- positive
Anti- HBs -negative
Anti- HBc - positive
Anti- HBc (IgM)- negative
ii. HCV
Viral clearance with long-term CM immunity occurs in (25%) while it usually
causes chronic infection in (75% of infections) where it presents due to persistent
viremia& hepatic inflammation/fibrosis.
Chronic presentations:
Cirrhosis: (10-20% of chronic infections)
Hepatocellular carcinoma: (1-5%). HCV is responsible for about 25% of HCC
cases.
d. TRANSMISSION OF HEMORRHAGIC FEVER VIRUSES TO
HUMANS
The viruses can be transmitted from animals to humans. Rodents and
arthropods main reservoir. Humans can be infected via bite of infected
arthropod, inhalation of rodent excreta, or contact with infected animal
carcasses, blood or secretions.
Person-to-person transmission possible with several agents. Primarily via

blood or bodily fluid exposure. Rare instances of airborne transmission with
arenaviruses and filoviruses
e. HERPES SIMPLEX VIRUS 1
Herpes simplex virus 1 is from the family, Herpesviridae, and sub-family,
alpha herpesvirinae.
Transmission of HSV-1, Via intimate contact (skin to skin contact), The virus
does not penetrate intact skin, Mild abrasion or chapping of skin can allow
infection.
Causes 95% of orofacial herpes and 10 -30% of primary genital herpes (but
seldom recurs there). It infects Oropharyngeal mucosal cells. The infection can
spread to different organs in the body which is known as Viremic spread.
Conditions include Acute gingivostomatitis, Recurrent herpes labialis (cold
sores), Keratoconjunctivitis, Encephalitis/meningitis, Pharyngitis,
Mucocutaneus lesions, herpetic whitlow. It has a lifelong latency in the
trigeminal ganglion.
Treatment: Antiviral medications, such as acyclovir, famciclovir, and
valacyclovir, are the most effective medications available for people infected
with HSV. These can help to reduce the severity and frequency of symptoms,
but cannot cure the infection.
Prevention: People with active symptoms of oral herpes should avoid oral
contact with others and sharing objects that have contact with saliva. They
should also abstain from oral sex, to avoid transmitting herpes to the genitals of
a sexual partner. Individuals with symptoms of genital herpes should abstain
from sexual activity whilst experiencing any of the symptoms.
The consistent and correct use of condoms can help to prevent the spread of
genital herpes.
Pregnant women with symptoms of genital herpes should inform their health
care providers. Preventing acquisition of a new genital herpes infection is
particularly important for women in late pregnancy, as this is when the risk for
neonatal herpes is greatest.
f. PATHOGENESIS OF HEPATITIS A VIRUS
• Feco oral transmission
• Replicates in enterocytes
• Spreads to liver and multiples in the hepatocytes
• Triggers cell-mediated hepatocellular destruction
• Excreted in faeces
• Causes transient viremia
a. LAB DIAGNOSIS OF HIV INFECTION TESTS AND FOR EACH TEST,
CITE ITS ADVANTAGE AND DISADVANTAGE
Virus Isolation:
HIV can be cultured from lymphocytes in peripheral blood (and occasionally

from specimens from other sites). Higher titers of virus are found in the plasma
and in peripheral blood cells of patients with AIDS as compared with
asymptomatic individuals. The magnitude of plasma viremia can be used to
correlate of the clinical stage of HIV infection which is better than checking for
presence of any antibodies. The most sensitive virus isolation technique is to
co-cultivate the test sample with uninfected, mitogen stimulated peripheral
blood mononuclear cells. The vast majority of HIV-1 antibody-positive persons
will have virus that can be cultured from their blood cells. However, a
disadvantage is that virus isolation techniques are time-consuming and
laborious and are limited to research studies.
Serology:
Test kits are commercially available for measuring antibodies by enzyme-
linked immunoassay (EIA). If properly performed these tests have a sensitivity
and specificity exceeding 98%.
The response pattern against specific viral antigens changes over time as
patients progress to AIDS. Simple, rapid tests for detecting HIV antibodies are
available for use in laboratories ill-equipped to perform EIA tests and in settings
where test results are desired with little delay. The simple tests can be
performed on blood or oral fluid. There are rapid tests that can detect HIV
antibodies in whole blood specimens that require no processing. These tests can
be performed outside the traditional laboratory setting. Home testing kits are
available. Most individuals will have detectable antibodies within 6–12 weeks
after infection, whereas virtually all will be positive within 6 months.
Disadvantage of this test is that the time lag between onset of infection and the
development of antibodies to the infecting microorganism results in the
possibility for false negative results.
Detection of Viral Nucleic Acid or Antigens:
Amplification assays such as the RT-PCR, DNA PCR, and bDNA tests are
commonly used to detect viral RNA in clinical specimens. The RT-PCR assay
uses an enzymatic method to amplify HIV RNA; the bDNA assay amplifies
viral RNA by sequential oligonucleotide hybridization steps. These molecular-
based tests are very sensitive and form the basis for plasma viral load
determinations. HIV sequence heterogeneity may limit the sensitivity of these
assays to detect HIV infections. The HIV RNA levels are important predictive
markers of disease progression and valuable tools with which to monitor the
effectiveness of antiviral therapies. Dried blood spot specimens are an
alternative to plasma specimens for viral monitoring in resource-limited
settings.
b. DIFFERENCES BETWEEN HUMAN PAPILLOMA VIRUS VACCINE
(GARDASIL) AND SALK POLIO VACCINE
HPV vaccine (GARDASIL) is a sterile preparation for intramuscular injection
and contains purified inactive proteins from HPV types 6, 11, 16, and 18. The
proteins in Gardasil are structural, virus-like proteins (VLP) that resemble the
HPV virus. The proteins can activate the immune system but cannot give rise
to replicating virus. Its classified as a subunit or recombinant vaccine which
involves using important parts of the virus to stimulate the immune system.
SALK is a polio vaccine that contains three serotypes of poliovirus inactivated
by treatment with formaldehyde and is administered by intramuscular
injection. Its classified as an inactivated vaccine (killed whole virus), where the
disease-causing microbe is killed with chemicals, heat, or radiation.
c. MECHANISM OF ACTION OF GANCICLOVIR
Ganciclovir's antiviral activity inhibits virus replication. This inhibitory action
is highly selective as the drug must be converted to the active form by a virus-
encoded cellular enzyme, thymidine kinase (TK). TK catalyzes
phosphorylation of ganciclovir to the monophosphate, which is then
subsequently converted into the diphosphate by cellular guanylate kinase and
into the triphosphate by a number of cellular enzymes. In vitro, ganciclovir
triphosphate stops replication of herpes viral DNA. When used as a substrate
for viral DNA polymerase, ganciclovir triphosphate competitively inhibits
dATP leading to the formation of 'faulty' DNA. This is where ganciclovir
triphosphate is incorporated into the DNA strand replacing many of the
adenosine bases. This results in the prevention of DNA synthesis, as
phosphodiester bridges can longer to be built, destabilizing the strand.
Ganciclovir inhibits viral DNA polymerases more effectively than it does
cellular polymerase, and chain elongation resumes when ganciclovir is
removed.
d. EPIDEMIOLOGY OF ROTA B VIRUS
Rotavirus gastroenteritis is caused by rotavirus that infects the stomach and
bowel. Rotavirus gastroenteritis is common in infants and young children.
Children under five years of age, especially those between 6 months and two
years are most vulnerable to the disease.
Rotavirus is highly contagious among children. Repeat infections with different
viral strains are possible, and most children have several episodes of rotavirus
infection in the first years of life. The first infection tends to be the most severe
as the body builds up immunity (resistance) to the virus afterwards. This is why
rotavirus infections are extremely rare in adults.
The incubation period for a rotavirus lasts approximately two days. Infants and
children with rotavirus infection have diarrhea, vomiting, fever and often
followed by abdominal pain and dehydration. Children - particularly those
under the age of two- are at higher risk of dehydration and may require hospital
treatment.
Infected people pass the virus before and after they have symptoms of the
illness. Infection results from ingestion of infected foods or drinks. Touching a
surface contaminated with rotavirus and then touching the mouth area can result
in infection.
The virus is highly resistant in the environment and can survive for months in
stools at room temperature. The virus is widespread in developing and
developed countries.
e. FACTORS ASSOCIATED WITH SEVERE RESPIRATORY
SYNCYTIAL VIRUS (RSV)
• Virtually all children get an RSV infection by the time they are 2 years old.
Most of the time RSV will cause a mild, cold-like illness, but it can also
cause severe illness such as: Bronchiolitis, Pneumonia. Those at greatest
risk for severe illness from RSV include:
o Premature infants
o Very young infants, especially those 6 months and younger
o Children younger than 2 years old with chronic lung disease
o Children younger than 2 years old with chronic heart disease
o Children with weakened immune systems
o Infants with severe congenital and acquired immune deficiency
syndromes may demonstrate prolonged viral shedding in RSV LRTI
and are reported to have increased morbidity and mortality
associated with RSV infection.
o Children who have neuromuscular disorders, including those who
have difficulty swallowing or clearing mucus secretions
• Adults at highest risk for severe RSV infection include:
o Older adults, especially those 65 years and older
o Adults with chronic heart or lung disease
o Adults with weakened immune systems
• Factors predisposing to a more severe course of RSV disease in
neuromuscular diseases include: The impaired ability to clear secretions
from the airways due to:
o Ineffective cough
o Respiratory muscle weakness
o High prevalence of gastro-esophageal reflux
o Swallowing dysfunction which leads to aspiration.
• Similarly, pulmonary disease is a common presenting feature and
complication of T-cell immunodeficiency.
a. PATHOGENESIS OF HEPATITIS B VIRUS
• Transmission: Sexual contact (Predominant mode among adults), Close
contact, Vertical transmission (during delivery, rarely transplacental, no
evidence of transmission through breastfeeding), Blood (transfusions,
Sharing of needles, razors, Tattooing, acupuncture, Renal dialysis, Organ
transplant)
• Replication: Infects and replicates in Hepatocytes
• Spread: Virus particles & surface protein released into blood, viremia is
prolonged and blood is highly infectious
• Host immune response: Viral antigens are displayed on infected

hepatocytes; cytotoxic T cells mediate an immune attack against the viral
antigens and destroys infected hepatocytes. Inflammation and necrosis
occur
• Disease mechanism: Level of immune response determines
manifestations: Chronic infection >> destruction/regeneration
>>cirrhosis/cancer: Virus enters in the (blood). Therefore, hepatitis B
pathogenesis is probably due to immune attack.
• Hepatocellular Carcinoma due to: Malignant transformation due to
insertional mutagenesis as HBV genome integrate into hepatocyte DNA.
Integration can activate cellular oncogene, loss of growth control (hence
cancer)
b. LABORATORY DIAGNOSIS OF HIV-1 INFECTION IN THE
NEWBORN
Virologic assays (i.e., HIV RNA or HIV DNA nucleic acid tests [NATs]) that
directly detect HIV must be used to diagnose HIV in infants and children aged
<18 months with perinatal and postnatal HIV exposure; HIV antibody tests
should not be used. A positive virologic test should be confirmed as soon as
possible by repeat virologic testing. The first HIV test should be performed at
14 to 21 days after birth, the second test at 1 to 2 months, and the third test at 4
to 6 months.
c. PATHOGENESIS OF HUMAN HERPES VIRUS-3 (HHV3)
Human herpes Virus-3 is also known as the varicella-zoster virus.
Varicella - The route of infection is the mucosa of the upper respiratory tract
or the conjunctiva. After initial replication in regional lymph nodes, primary
viremia spreads virus and leads to replication in the liver and spleen. Secondary
viremia involving infected mononuclear cells transports virus to the skin, where
the typical rash develops. Swelling of epithelial cells, ballooning degeneration,
and the accumulation of tissue fluids result in vesicle formation. Varicella-
zoster virus replication and spread are limited by host humoral and cellular
immune responses. Interferon is likely involved also. It has been shown that a
varicella-zoster virus-encoded protein, ORF61, antagonizes the β-interferon
pathway. This presumably contributes to the pathogenesis of viral infection.
Zoster- The skin lesions of zoster are histo-pathologically identical to those of
varicella. There is also an acute inflammation of the sensory nerves and ganglia.
Often only a single ganglion may be involved. As a rule, the distribution of
lesions in the skin corresponds closely to the areas of innervation from an
individual dorsal root ganglion. It is not clear what triggers reactivation of latent
varicella-zoster virus infections in ganglia. It is believed that waning immunity
allows viral replication to occur in a ganglion, causing intense inflammation
and pain. Virus travels down the nerve to the skin and induces vesicle
formation. Reactivations are sporadic and recur infrequently.
d. LAB DIAGNOSIS OF HEPATITIS B INFECTION
Based on serum markers: HBsAg, Anti-HBs, Anti-HBc, HBeAg, Anti-Hbe,

HBV-DNA:
• Surface antigen (HBsAg) - secreted in excess into the blood. Presence in
serum = virus replication in liver
• 'e' antigen (HBeAg) - shed in small amounts into the blood. Presence in
serum = high level of viral replication liver
• Core antigen (HBcAg) core protein - not found in blood
Serological diagnosis and indications:
• HBsAg: used as a general marker of infection.
• HBsAb: used to document recovery and/or immunity to HBV infection.
• Anti-HBc IgM: marker of acute infection.
• Anti-HBcIgG: past or chronic infection.
• HBeAg: indicates active replication of virus and therefore infectiveness.
• Anti-Hbe: virus no longer replicating. However, the patient can still be
positive for HBsAg which is made by integrated HBV.
• HBV-DNA: indicates active replication of virus, more accurate than
HBeAg especially in cases of escape mutants. Used mainly for monitoring
response to therapy.
e. CHARACTERISTICS OF HUMAN PAPILLOMAVIRUS
• Family: Papillomaviridae
• Small (8 kBp), circular dsDNA virus
• Non-enveloped
• Over 300 genotypes so far, 40 affect anogenital region
• HPV linked to anogenital, oropharyngeal cancer
18. LIST THE 5 TYPES OF HEPATITIS VIRUSES INDICATING THE NUCLEIC
ACID COMPONENT, MODES OF TRANSMISSION AND COMPLICATIONS
OF EACH
19. WRITE SHORT NOTES ON THE FOLLOWING:

a. HERPES SIMPLEX 1
Herpes simplex virus 1 is from the family, Herpesviridae, and sub-family, alpha
herpesvirinae. Transmission of HSV-1, Via intimate contact (skin to skin
contact), The virus does not penetrate intact skin, Mild abrasion or chapping of
skin can allow infection. Causes 95% of orofacial herpes and 10 -30% of
primary genital herpes (but seldom recurs there). It infects Oropharyngeal
mucosal cells. The infection can spread to different organs in the body which is
known as Viremic spread. Conditions include Acute gingivostomatitis,
Recurrent herpes labialis (cold sores), Keratoconjunctivitis,
Encephalitis/meningitis, Pharyngitis, Mucocutaneus lesions, herpetic whitlow.
It has a lifelong latency in the trigeminal ganglion.
b. RABIES VIRUS
Rabies causes inflammation of the brain. Most of the time it’s very fatal. It is
Present on all continents (except Antarctica) and 95% of all cases occur in
Africa and Asia. 99% of Human rabies is acquired from dogs. Examples of
other animals that humans can also acquire rabies from are bats, foxes, wolves,
racoons, skunks. Rabies is from the family, Rhabdoviridae and the Genus,
Lyssavirus. It’s a negative sense singled stranded RNA virus (Baltimore Group
V and is Enveloped. Spread by Bite/scratch/saliva from infected animal. Initial
replication is in myocytes. Long incubation period is based on size of inoculum
and distance from CNS. Enters peripheral nerves through myoneural junction.
Travels to ganglion and replicates and then travels to the brain. Causes rapidly
progressive encephalitis and spreads to periphery and salivary glands. Clinical
presentations are hyperactive, hydrophobia, aerophobia, gradual paralysis of
muscles, slow onset of coma and eventually death. Diagnostic tests are Serology
(Antibodies/antigens), PCR, Sequencing or Microscopy (e.g. negri bodies in
neurons).
c. MEASLES VIRUS
Genus: Morbilivirus
Family: Paramyxoviridae
Nucleic acid: (-) ssRNA, linear, enveloped
Transmission: Used to infect nearly everyone before vaccine was available
(1963). Transmitted through aerosol, direct contact. Affects humans only,
infection leads to life-long immunity
Clinical features: Fever, Respiratory symptoms: Coryza, cough,
conjunctivitis, Koplik’s spots on mucosae, Maculopapular rash extending from
face to extremities
Complications: Pneumonia, Encephalitis, Blindness
d. VIROLOGY, IMMUNOLOGY AND TREATMENT OF ROTAVIRUS
Virology:
• Causes viral gastroenteritis. Transmission is via fecal-oral route. High
numbers of viral particles are shed in diarrheal stools (1010/gm). Typical
symptoms include watery diarrhea, fever, abdominal pain, and vomiting,
• leading to dehydration.
• Classification of Rotaviruses: They belong to Reoviridae family.
Rotavirus has a segmented, double-stranded RNA genome surrounded by a
double-layered icosahedral capsid without an envelope. The rotavirus
genome has 11 segments
• Five species (A- E). Plus, two tentative species (F and G) based on antigenic
epitopes on the internal structural protein VP6. Virus of group B found only
in China. Group A is important human pathogen. Outer capsid protein VP4
and VP7 carry epitopes important in neutralizing antibodies.
• Importance of Rotaviruses: Major cause of diarrheal illness in infants in
the world. Adults too can get infected.
Immunology:
• Summary of Replicative Cycle: Rotavirus attaches to the cell surface at
the site of the β-adrenergic receptor. After entry of the virion into the cell,
the RNA-dependent RNA polymerase synthesizes mRNA from each of the
11 segments within the cytoplasm. The 11 mRNAs are translated into the
corresponding number of structural and nonstructural proteins. One of
these, an RNA polymerase, synthesizes minus strands that will become part
of the genome of the progeny virus. Capsid proteins form an incomplete
capsid around the minus strands, and then the plus strands of the progeny
genome segments are synthesized. The virus is released from the cytoplasm
by lysis of the cell, not by budding.
• The glycoprotein VP7 defines the G serotypes and the protease-sensitive
protein VP4 defines P serotypes.
o VP1 is RNA polymerase
o VP2 binds the polymerase

o VP3 is a capping enzyme, guanylyl transferase, that catalyses the
formation of the 5' cap
o VP4 is on the surface of the virion that protrudes as a spike. It binds
to β-adrenergic receptors and drives the entry of the virus into the
cell.
o VP4 has to be modified by the protease enzyme trypsin, which is
found in the gut, into VP5 and VP8 before the virus is infectious.
VP4 determines how virulent the virus is and the P-type of the virus
o VP6 forms the bulk of the capsid. It is highly antigenic and can be
used to identify rotavirus species. This protein is used in laboratory
tests for rotavirus A infections.
o VP7 is a glycoprotein that forms the outer surface of the virion.
Apart from its structural functions, it determines the G-type of the
strain and, along with VP4, is involved in immunity to infection. It's
the predominant antigen
• Immunity: Intestinal secretory IgA directed against specific serotypes

protects against reinfection and colostrum IgA protects newborns up to the
age of 6 months. Highest conc. of IgA is found on mucosal surfaces
naturally
Treatment: Treatment of Gastroenteritis is supportive by correction of Loss of

water and electrolytes. Failure for prompt correction of dehydration leads to
Acidosis, Shock, Death.
Vaccine: oral live attenuated pentavalent human–bovine reassortant rotavirus
vaccine (Rotateq), which contains five rotavirus strains, and an oral live
attenuated monovalent (Rotarix) human rotavirus vaccine, which contains the
single most common rotavirus serotype (G1). Both vaccines are safe and
effective, and neither is associated with intussusception.
20. WRITE SHORT NOTES ON THE TYPES OF VACCINES, GIVING
EXAMPLES IN EACH CASE AND THE COMPLICATIONS ASSOCIATED
WITH IMMUNE-PROPHYLAXIS
• Live whole virus vaccines: Live/attenuated whole virus, also called
modified live vaccines. Uses pathogens that are living but have reduced
virulence so they don't cause disease. Approach for producing attenuated
viruses; Repeated passage in cell culture, Temperature-sensitive, Deletion
mutants. Examples include: Measles, mumps, rubella (MMR combined
vaccine), Rotavirus, Smallpox, Chickenpox, Yellow fever
• Killed whole virus vaccines: In inactivated vaccines, the disease- causing
microbe is killed with chemicals, heat, or radiation. Examples: Hepatitis A,
Flu (shot only), Polio (shot only), Rabies.
• Subunit and recombinant vaccines; uses important parts of the virus to
stimulate the immune system. They are used to protect against: Hib
(Hemophilus influenzae type b) disease, Hepatitis B, HPV (Human
papillomavirus), Whooping cough (part of the DTaP combined vaccine),
Pneumococcal disease, Meningococcal disease, Shingles.
o Purified: the peptide may be identified from the virus, isolated then
purified. Characteristics of Peptide vaccines: The chances of an
adverse reaction to the vaccine are lower. Downside: identifying the
precise antigens which best stimulate the immune system is difficult
and time-consuming.
o Recombinant virus vaccines: Due to the above downside, it may
be possible to manufacture the antigen molecules using recombinant
DNA technology.
• DNA vaccines: DNA vaccines uses the naked DNA from a few genes of
the invading organism. Those genes are introduced into the body, taken up
by some of the cells. Those host cells would then produce the antigens
molecules, allowing them to be displayed and stimulating the Immune
system.
a. ASYMPTOMATIC STAGE OF HIV INFECTION
This stage of HIV infection does not cause outward signs or symptoms. A
person may look and feel well but HIV is continuing to weaken their immune
system. This stage may last months to several years (an average of 8 to 10 years)
and without a HIV test many people do not know they are infected. It occurs
due to low or absent viremia. One may present with lymphadenopathy and with
CD4 titers of >500 cells/mm3
b. ALPHA-HERPES VIRUSES
Alpha herpes viruses are a sub-family of the Herpesviridae family. The genus
of this sub-family includes the simplex virus, which comprises of the simplex-
1 and 2, and the varicelovirus which includes the varicella zoster virus. Diseases
caused by alpha-herpes viruses are orofacial lesions, genital lesions and chicken
pox which recurs as shingles. Their site of latency is the sensory nerve ganglia.
c. 5 OPPORTUNISTIC INFECTIONS ASSOCIATED WITH HIV
• Pneumonia
• Kaposi’s sarcoma
• Cryptococcal meningitis
• Thrush
• Pneumocystic pneumonia
• Toxoplasmosis
• Cytomegalovirus
• Esophageal candidiasis
d. CHARACTERISTICS SHARED BY ALL VIRAL HEMORRHAGIC
FEVER VIRUSES
• Single stranded RNA that is enveloped
• Require a reservoir host to survive such as mosquitos
• Are limited to the geographical location of the reservoir host
• They have no cure
• Sporadic and irregular human outbreaks

e. DIFFERENTIATE LOCALIZED VS SYSTEMIC INFECTION USING
SPECIFIC VIRUSES AS EXAMPLES
Localized infection is characterized by infection and initial replication n the
epithelial cells i.e. site of entry. For example, HPV infects the epithelial cells of
the cervix. The spread of infection is via sequential infection of neighboring
cells.
Systemic infections, also known as generalized infections, characterized by
infection and replication at the site of infection followed by spread via
lymphatics i.e. regional lymph nodes. Primary viremia is at target organs
followed by a secondary viremia which could result in virus spread to other
parts of the body. For example, Polio
22. LIST 5 VIRUSES AND THEIR MODES OF TRANSMISSION ASSOCIATED
WITH CNS INFECTIONS
Polio virus – Feco-oral
Rabies – Animal bites/scratches
Mumps – close contact
West Nile – Mosquitos (anthropods)
HSV-2 – Sexual intercourse
23. THERE ARE 3 MAJOR ASPECTS OF VIRUS PATHOGENESIS:
a. LIST AND DISCUSS EACH OF THEM IN DETAILS, GIVING
SPECIFIC EXAMPLES
They include both cellular & viral factors:
1. Viral virulence: Ability to promote replication & cell change -> Measure of
pathogenicity
2. Host genetic factors: Presence/absence of receptors (e.g CCR5 delta32 in
HIV), Age (young vs. old)
3. Immunological status: Normal vs. Immunocompromised, Primary vs.
secondary infection, Pre-existing immunity (due to vaccination/prior infection),
Dual infection
a. PATHOGENESIS OF RABIES VIRUS
Rabies virus multiplies in muscle or connective tissue at the site of inoculation
and then enters peripheral nerves at neuromuscular junctions and spreads up the
nerves to the central nervous system. However, it is also possible for rabies
virus to enter the nervous system directly without local replication. It multiplies
in the central nervous system and progressive encephalitis develops. The virus
then spreads through peripheral nerves to the salivary glands and other tissues.
The organ with the highest titers of virus is the submaxillary salivary gland.
Other organs where rabies virus has been found include pancreas, kidney, heart,
retina, and cornea. Rabies virus has not been isolated from the blood of infected
persons. Susceptibility to infection and the incubation period may depend on
the host’s age, genetic background, and immune status, the viral strain involved,
the amount of inoculum, the severity of lacerations, and the distance the virus
has to travel from its point of entry to the central nervous system. There is a
higher attack rate and shorter incubation period in persons bitten on the face or
head; the lowest mortality occurs in those bitten on the legs. Rabies virus
produces a specific eosinophilic cytoplasmic inclusion, the Negri body, in
infected nerve cells. Negri bodies are filled with viral nucleocapsids. The
presence of such inclusions is pathognomonic of rabies but is not observed in
at least 20% of cases. Therefore, the absence of Negri bodies does not rule out
rabies as a diagnosis.
b. GENERAL CHARACTERISTIC PROPERTIES OF RETROVIRUSES
(USE HIV-1 AS AN EXAMPLE)
• Genomes consist of two copies of +ve sense stranded RNA. For HIV
Baltimore class 6 (ssRNA + Reverse Transcriptase)
• Undergo reverse transcription followed by chromosomal integration
• Diploid RNA
• Integrated DNA co-linear with viral DNA
• Associated with tumors, leukemias and immunodeficiencies
• Have 3 common gene: GAG, POL & ENV
c. CLASSIFICATION OF HIV-1 BASED ON CO-RECEPTOR USAGE
HIV infects CD4(+) cells of the immune system (T cells, monocyte-
macrophages and dendritic cells) via interaction with a universal primary
receptor, the CD4 molecule, followed by a mandatory interaction with a second
receptor (co-receptor) belonging to the chemokine receptor family.
d. THERAPIES USED IN CONTROL OF HIV-1

e. VIRAL AGENTS TRANSMITTED VIA VECTORS
i. CHOOSE ONE OF THE AGENTS FROM THE LIST AND

DISCUSS ITS PATHOGENESIS
Dengue fever - The pathogenesis of the severe syndrome involves pre-
existing dengue antibody. It is postulated that virus–antibody complexes
are formed within a few days of the second dengue infection and that
the non-neutralizing enhancing antibodies promote infection of higher
numbers of mononuclear cells followed by the release of cytokines,
vasoactive mediators, and procoagulants, leading to the disseminated
intravascular coagulation seen in the hemorrhagic fever syndrome.
Cross-reactive cellular immune responses to dengue virus may also be
involved.
Yellow fever - The virus is introduced by a mosquito through the skin,
where it multiplies. It spreads to the local lymph nodes, liver, spleen,
kidney, bone marrow, and myocardium, where it may persist for days.
It is present in the blood early during infection. The lesions of yellow
fever are caused by the localization and propagation of the virus in a
particular organ. Infections may result in necrotic lesions in the liver
and kidney. Degenerative changes also occur in the spleen, lymph
nodes, and heart. Serious disease is characterized by hemorrhage and
circulatory collapse. Virus injury to the myocardium may contribute to
shock.
25. LIST 3 FAMILIES OF VIRUSES WHERE ANTIVIRAL AGENTS ARE USED
FOR TREATMENT
a. FOR EACH FAMILY LISTED ABOVE, PICK AN ANTIVIRAL AGENT
USED AND DISCUSS ITS MECHANISM OF ACTION IN DETAIL
Anti-herpesvirus agents:
• Acyclovir, Valacyclovir/ Ganciclovir/ Valganciclovir/ Famciclovir,
Foscarnet, Fomiversen, Docosanol
Anti-influenza agents:
• Uncoating Inhibitors (Amantadine, Rimantadine), Viral release
inhibitors (Oseltamivir, Zanamivir, Peramivir), RNA Polymerase
Inhibitors (Ribavirin, Favipravir)
Anti-hepatitis B virus agents:
• Immunomodulant [Interferon (IFN)], HBV DNA Polymerase Inhibitors
(Entecavir, Tenofovir, Lamivudine, Telbivudine, Adefovir)
Anti-Hepatitis C virus agents:
• Immunomodulant (Interferon), RNA Polymerase Inhibitors (Ribavirin,
Sofosbuvir, Dasabuvir), Protease Inhibitors (Simeprevir, Paritaprevir,
Grazoprevir), NS5A Inhibitors (Daclatasvir, Ledipasvir, Velpatasvir,
Ombitasvir, Elbasvir)
Anti-retroviral agents (ARVs):
• Attachment blocker – Maraviroc, Fusion Blocker – Enfuvirtide, Reverse
transcriptase inhibitors; Nucleoside analogues — Zidovudine,
Lamivudine, Non-Nucleoside analogues — Efavirenz, Nevirapine,
Etravirine, Integration inhibitors — Raltegravir, Dolutegravir, Protease
inhibitors — Ritonavir, Lopinavir

a. LABORATORY METHODS FOR DIAGNOSIS OF VIRAL
INFECTIONS AND THE PRINCIPLES BEHIND THEIR USE
Three General Approaches for Laboratory Diagnosis of Viral Infections:
• Virus Isolation (Indirect Examination): CPE and other characters, Animal
systems (Eggs, mice etc.)
• Direct detection: Microscopy or staining, Detection of nucleic acid, antigens
• Serology: Antibodies (Indirect), Antigen (Direct)
Direct Detection of Virus:
• Electron Microscopy: Morphology of virus particles, Immune electron
microscopy.
• Light Microscopy: Histological appearance, Inclusion bodies
• Antigen Detection: Immunofluorescence Assay (IFA); Use monoclonal
antibodies (MoAbs) labelled with a fluorescent dye, MoAbs bind to specific
epitope on viral protein, visualize infected cells using fluorescent
microscopy, Only virus-infected cells will fluoresce, ELISA etc.
• Viral Genome Detection: Hybridization with specific nucleic acid probes,
Polymerase chain reaction (PCR)
Detection of Viral Proteins:
• Quantitative plaque assay: Plaque Assays is a virological assay employed

to count and measure the infectivity level of viruses. The basis of plaque
assay is to measure the ability of a single infectious virus to form a “plaque”
on a concurrent monolayer culture cell. It is cell culture-based and used for
lytic viruses only. Steps: Serial dilution of virion-containing solution,
create tissue culture plates, spread diluted virus, overlay with agar to prevent
diffusion, Count number of plaques, each plaque represents IPFU (Plaque
Forming Unit)
• Viral Hemagglutination: Some viruses and microbes contain proteins
which bind to erythrocytes (red blood cells) causing them to clump together
Paramyxoviruses e.g. mumps, measles, Parainfluenza, Influenza virus,
Adenovirus. Readings The results: Titer: The maximum dilution that gives
visible agglutination. The end point: is the well with the lowest
concentration of the virus where there is hemagglutination
Virology Serology:
• Enzyme-Linked Immunosorbent Assays (ELISAs): Enzyme reacts with
substrate -> colored product. Substrate initially colorless. Color intensity is
both quantitative and qualitative. Antigen used e.g p24 for HIV infection. It
is very sensitive. In HIV test: If positive twice, Western Blotting is
performed next. Detection of antigen (Antigen ELISA) — Direct Detection
of antibodies (Ab ELISA) — Indirect test.
• Western Blotting: Viral proteins are separated In SDS poly-acryl gel

electrophoresis (PAGE gel), Transferred to a nitrocellulose filter, detected
by labeled antibodies. Patient sample loaded onto gel, Electric current is
then applied, SDS ensures equal negative charge. Smallest proteins migrate
longest distance, all proteins in gel are transferred to paper (nitrocellulose),
Paper is probed with specific antibodies
• Southern blotting: DNA- starting material, Restriction Enzyme digestion,
Resolve DNA fragments on agarose gel, Transfer DNA from gel ->
nitrocellulose membrane (NM), Probe for target DNA with radio-labelled
oligonucleotide probe, Expose NM to X-ray film, Develop X-ray film,
Observe DNA bands
• Restriction-fragment length polymorphism (RFLP): Cut genomic DNA
from two individuals with restriction enzyme, Run Southern blot, probe
with different pieces of DNA, Sequence difference creates different band
pattern, Compare bands. Applications: Catching the bad guys, DNA
fingerprinting
• Northern blot analysis: similar to southern blot but uses RNA instead of
DNA as the starting material
• Polymerase-Chain Reaction (PCR): Ingredients: DNA (template) e.g.
from patient, Primers, DNA polymerase (Taq polymerase), Nucleotides (A,
C, G, T) Steps: Denaturation (95C), Annealing (55C), Extension (72C)
Virus Isolation — Cell cultures:
• Three types:
o Primary cells e.g. Monkey Kidney
o Semi-continuous cells e.g. Human embryonic kidney and skin
fibroblasts
o Continuous cells e.g. HeLa, Vero
b. WHICH LABORATORY METHOD WOULD YOU USE IN THE
DIAGNOSIS OF HIV-1 IN A 6-MONTH OLD BABY BORN TO AN HIV-
1 INFECTED MOTHER AND WHY WOULD YOU CHOOSE THIS
METHOD?
Virologic assays (i.e., HIV RNA or HIV DNA nucleic acid tests [NATs]) that
directly detect HIV must be used to diagnose HIV in infants and children aged
<18 months with perinatal and postnatal HIV exposure. Antibody testing in a
newborn is not an accurate way to determine whether HIV infection has
occurred in the infant. HIV antibody tests, including newer tests, do not
establish the presence of HIV infection in infants because of transplacental
transfer of maternal antibodies to HIV. Virologic HIV tests, however, look
directly for HIV in the blood and therefore should be used. Antigen ELISA can
therefore be employed.
c. STRATEGIES FOR CONTROL OF A HUMAN INFLUENZA
EPIDEMIC
1.Surveillance
2. Screening
3. Information sharing
4. Health education
5. Health worker capacity

6. Drugs (Prophylaxis)
7. Vaccination (annual)
8. Culling animals (chicken/swine)
9. Limiting travel
10. Isolation of infected person
27. BRIEFLY DISCUSS VIRAL HEPATITIS B UNDER THE FOLLOWING
SUBHEADINGS:
a. CLINICAL DIAGNOSIS
Acute hepatitis B is a clinical diagnosis identified by the detection of HBsAg,
symptoms, high serum aminotransferases. Usually anti-HBc IgM can be
detected and HBV DNA is present. HBeAg can also be identified in most acute
phase of infections, but has little clinical importance. The diagnosis of chronic
infection is based on the persistence of HBsAg for more than 6 months. Patients
with chronic HBV infection are commonly diagnosed by laboratory means but
not by clinical presentations. Past HBV infection is defined by the coexistence
of anti-HBs and IgG anti-HBc.
b. LAB DIAGNOSIS OF ACUTE DISEASE
The diagnosis of HBV infection requires the evaluation of the patient's blood
for HBsAg, hepatitis B surface antibody (HBsAb), and hepatitis B core
antibody (HBcAb). Although the presence of HBsAg indicates that the person
is infectious, the presence of HBsAb indicates recovery and immunity from
HBV infection or successful immunization against HBV. HBcAb appears at the
onset of acute HBV infection, but may also indicate chronic HBV infection.
HBV DNA sometimes may be the only marker present in early infections.
28. DESCRIBE ANTIGENIC VARIATION IN INFLUENZA A VIRUS
Antigenic drift:
▪ Occurs in all Influenza viruses
▪ Gradual accumulation of mutations
▪ May generate a new strain
▪ Acquired immunity is no longer effective
▪ Causes seasonal outbreaks and limited epidemics. Antigenic
Shift:
▪ Mainly occurs in Influenza A
▪ Due to re-assortment of RNA segments
▪ Occurs in a cell infected with different sub-types
▪ May lead to a new virus subtype
▪ No previous immunity to the new sub-type
▪ Causes sporadic epidemics/pandemic
29. LIST 5 TYPES OF CANCERS CAUSED BY VIRUSES. CLEARLY INDICATE
THE CANCER TYPE AND CORRESPONDING VIRUS
Burkitt's Lymphoma – Epstein-Barr Virus (EBV)
Kaposi's Sarcoma - Human Herpesvirus 8 (HH8)
Cervical Cancer, Head and Neck Cancers, Anal, Oral, Pharyngeal, and Penile Cancers
- Human Papillomavirus (HPV)
Adult T-cell Leukemia - Human T-cell Lymphotropic Virus 1 (HTLV)
Merkel Cell Carcinoma (Skin Cancer) - Merkel Cell Polyomavirus (MCP)
a. OUTLINE 5 ORAL MANIFESTATIONS OF HIV
HIV makes a patient immunodeficient increasing risks of getting these
infections:
Candidiasis - Oral candidiasis is most commonly associated with Candida
albicans, although other species, such as C. glabrata and C. tropicalis, are
frequently part of the normal oral flora. The most common presentations
include pseudomembranous and erythematous candidiasis, which are equally
predictive of the development of AIDS. These lesions may be associated with
a variety of symptoms, including a burning mouth, problems eating spicy food,
and changes in taste.
Hairy leukoplakia (EBV): Oral hairy leukoplakia presents as a non-movable,
corrugated or "hairy" white lesion on the lateral margins of the tongue. The
lesions can be unilateral or bilateral.
Kaposi sarcoma (HHV-8): Kaposi's sarcoma may occur intraorally, either
alone or in association with skin and disseminated lesions. Intraoral lesions
have been reported at other sites and may be the first manifestation of late-stage
HIV disease (AIDS). The most common oral site is the hard palate, but lesions
may occur on any part of the oral mucosa.
Periodontitis: Periodontal disease is a fairly common problem in both
asymptomatic and symptomatic HIV-infected patients. It can take two forms:
the rapid and severe condition called necrotizing ulcerative periodontitis and its
associated and possibly precursor condition called linear gingival erythema.
Occurs in clean mouths where there is very little plaque or calculus to account
for the gingivitis. The gingiva may be reddened and edematous and there can
be spontaneous bleeding.
Oral warts (HPV): HPV lesions in the oral cavity may appear as solitary or
multiple nodules. They may be sessile or pedunculated and appear as multiple,
smooth-surfaced raised masses resembling focal epithelial hyperplasia or as
multiple, small papilliferous or cauliflower-like projections
b. LIST 5 CHARACTERISTICS OF POLIO VIRUS
• Polio virus comes from the Picornaviridae family
• They are enteroviruses.
• They are positive sense single stranded RNA
• Polio is a naked virus
• They are transmitted feco-orally
c. LIST 5 RISK FACTORS FOR ACQUISITION OF HUMAN
HERPESVIRUS TYPE 2 (HHV-2)
• Human herpesvirus type 2 (HHV-2) is also known as Herpes simplex Virus

2 (HSV-2).
• Older aged people are at a higher risk of being infected by HHV-2.
• Women are more at risk at getting the virus than men.
• People who are not well educated will not know much about the
transmission and prevention of the virus and are more likely to be infected.
• People with poor socioeconomic status don’t have access to good education
and may not be able to afford things that help prevent the spread of viruses
like contraceptives.
• People with higher number of lifetime sexual partners increase the chances
of acquiring HHV-2.
• Prior sexually transmitted disease increases the risk of getting HHV-2. For
example, if a person has HIV, they become immunocompromised making
it more likely for them to be infected by HHV-2 because they don’t have a
strong immune system.
d. HOST IMMUNE RESPONSE EVENTS FOLLOWING A VIRAL
INFECTION
• Immune responses to viral infections: Innate immunity, Adaptive T-cell
immunity, Adaptive B-cell immunity
• Innate immunity to viruses: Composed of; Physical barriers (the skin,
mucus lining the mucosal membranes, tears). Soluble components:
Interferon, Cytokines, Chemokines, Complement Cells -Macrophages,
Dendritic cells and Natural killer cells (NK). Interferon: Interferons are
host proteins induced by virus in vertebrates that interfere with viral
replication (type 1). There are 3 different classes of interferon (IFN): α β,
and γ; α and β are called type I interferon, function mainly in inducing cells
to become resistant to viral infections γ is type II interferon, functions to
mainly to modulate the immune response
• Humoral immunity: Virus neutralization. In viremic infections, antibodies
neutralize virus, preventing its attachment to Receptor sites on susceptible
cells e.g. Poliovirus. Antibodies destroy free virus particles directly by:
Aggregation of virus and opsonization.
• Cell mediated immunity acts on virus infected cells through: CD8 (CTLS)
kill virus infected cells directly after recognition of viral antigens on cell
surface in association with MHC l. CD4 (T-Helper-cells) stimulated by viral
antigens release cytokines which attract and activate macrophages to kill
virus- Infected cells.
e. FACTORS THAT FAVOR DEVELOPMENT OF VIRAL
IMMUNOLOGICAL TOLERANCE

a. ROLE OF INTERFERONS IN VIRUS-INFECTED CELLS
Interferons are activated by double-stranded RNA, inhibition of cellular protein
synthesis, or enveloped virus. Initiates the antiviral state in surrounding cells.
Tried to prevent the next cell from getting infected. Blocks local viral
replication and then initiates systemic antiviral responses. Interferons are host
proteins induced by virus in vertebrates that interfere with viral replication (type
1). There are 3 different classes of interferon (IFN): α β, and γ; α and β are
called type I interferon, function mainly in inducing cells to become resistant to
viral infections γ is type II interferon, functions to mainly to modulate the
immune response
b. FORMS OF TRANSMISSION OF STIS GIVING EXAMPLES
c. RISK FACTORS FOR HSV-2
• Older age
• Female gender
• Poor socioeconomic
• Low level of education
• Prior sexually transmitted disease
• Higher number of lifetime sexual partners
BE STILL, DO NOT FEAR. LET IT SETTLE IN YOUR HEART THAT HE IS GOD. HE

IS THE BEGINNING AND THE END. HE THEREFORE SHALL SEE YOU FORTH IN
YOUR QUEST EVEN AS YOU SEEK TO BECOME THE GREAT PRACTITIONERS,
HE’S ORCHESTRATED FORTH FOR YOU TO BECOME. BARAKA!!!

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ISAAC OCHIENG’S REVISION SERIES

ANSWERS TO THE ASSORTED VIROLOGY SAQS FOR MBCHB/BDS

“WHERE GOD LEADS, HE PROVIDES. WHERE HE GUIDES, HIS

• Ribavirin- Inhibits the RNA polymerase of RNA viruses such as Hepatitis C

3. DESCRIBE BRIEFLY THE ADVANTAGES AND DISADVANTAGES OF

4. OUTLINE 5 DIFFERENCES BETWEEN HEPATITIS A AND C VIRUS

Variable Hepatitis A Hepatitis C

They are small proteinaceous Infectious particles that are resistant to

8. WRITE BRIEF NOTES ON THE FOLLOWING:

9. LIST 5 CLASSES OF ANTI-VIRAL AGENTS OTHER THAN ARVS, GIVING

10. WRITE SHORT ESSAYS ON THE FOLLOWING:

transmission as much as a 100-fold because the inflammation and sores

• Glucose cotransport of electrolytes is decreased but oral rehydration

• Asymptomatic Chronic Infection (carrier)

Person-to-person transmission possible with several agents. Primarily via

HIV can be cultured from lymphocytes in peripheral blood (and occasionally

• Host immune response: Viral antigens are displayed on infected

Based on serum markers: HBsAg, Anti-HBs, Anti-HBc, HBeAg, Anti-Hbe,

19. WRITE SHORT NOTES ON THE FOLLOWING:

o VP2 binds the polymerase

• Immunity: Intestinal secretory IgA directed against specific serotypes

Treatment: Treatment of Gastroenteritis is supportive by correction of Loss of

• Sporadic and irregular human outbreaks

d. THERAPIES USED IN CONTROL OF HIV-1

i. CHOOSE ONE OF THE AGENTS FROM THE LIST AND

26. BRIEFLY DISCUSS THE FOLLOWING:

• Quantitative plaque assay: Plaque Assays is a virological assay employed

• Western Blotting: Viral proteins are separated In SDS poly-acryl gel

5. Health worker capacity

• Human herpesvirus type 2 (HHV-2) is also known as Herpes simplex Virus

31. BRIEFLY DISCUSS THE FOLLOWING:

BE STILL, DO NOT FEAR. LET IT SETTLE IN YOUR HEART THAT HE IS GOD. HE

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