Professional Documents
Culture Documents
Helical Icosahedral
Viral Morphology
Enveloped Complex
Modes of Viral Multiplication
Coxsackie virus
Enteric human pathogenic orphan
COXSACKIE VIRUS
POLIO VIRUS
Paralysis or poliomyelitis
Septic meningitis with no
paralysis
OPV
Salk vaccine
Polio virus
POLIOMYELITIS
Dengue virus
Dengue fever
Breakbone fever
JBE
Yellow fever virus
Chikungunya virus
West Nile fever virus
Murray valley encephalitis virus
Myxo virus
Paramyxovirus
– Mumps virus
– Endemic parotitis
MUMPS
GENERAL DETAILS
Prevention
Virus related to Measles virus
MAN ONLY HOST
– LIVE ATTENUATED
ONE SEROTYPE VACCINE
SUB-CLINICAL INFECTIONS – DOES NOT SPREAD
CONTAGIOUS BEFORE AND TO CONTACTS
AFTER SYMPTOMS – Contradindicated in
Affects the Parotid glands
immune-
(Viral Parotitis) and may cause
orchitis that may lead to suppressed
infertility pregnant women
42
Orthomyxovirus
– Parainfluenza virus
– Respiratory syncitial virus
– Rhinovirus
– coronavirus
CORONAVIRIDAE
Severe Acute Respiratory Syndrome-
Associated Coronavirus (SARS)
Newly emerging disease – 2002
Transmitted through droplet or direct contact
Treatment is supportive.
47
AVIAN’S FLU
Influenza Virus
Pseudomyxovirus
Rubeola
– Measles
– Koplick’s spots ( oral lesion )
– SSPE
Rubella
– German measles
– Transplacental
RUBELLA VIRUS
TOGAVIRUS FAMILY
– Alphavirus genus
– Rubivirus genus
AEROSOL
CHILDREN, ADULTS
– mild
FETUS
– can be severe
53
Rubella
Two clinical forms:
Postnatal rubella – malaise, fever, sore
throat, lymphadenopathy, rash, generally
mild, lasting about 3 days
Congenital rubella – infection during 1st
trimester most likely to induce miscarriage
or multiple defects such as cardiac
abnormalities, ocular lesions, deafness,
mental and physical retardation
Diagnosis based on serological testing
No specific treatment available
Attenuated viral vaccine MMR
54
SYMPTOMS
SORE THROAT, RUNNY
NOSE, COUGH
FEVER
RASH, MINOR, IRREGULAR
– lasts 12hour to 5days
– not always seen
ARTHRALGIA, ARTHRITIS
– especially in adults,
especially women
LYMPHOADENOPATHY
55
EFFECTS ON FETUS
HEARING LOSS thrombocytopenia
CONGENITAL HEART
hepatomegaly
DEFECTS
splenomegaly
NEUROLOGICAL
– PYSCHOMOTOR intrauterine
AND/OR MENTAL growth retardation
RETARDATION
bone lesions
OPHTHALMIC
pneumonitis
– CATARACT,
GLAUCOMA,
RETINOPATHY
56
PREVENTION
LIVE ATTENUATED VACCINE
– DOES NOT SPREAD TO FAMILY
MEMBERS
– CHILDREN
– SUSCEPTIBLE NON-PREGANT
FEMALES
57
Transplacental effect
Possible chromosomal breakage
Inhibition of normal mitosis
Deafness
Congenital heart disease
Cerebral damage
Mental retardation
Occasionally glaucoma
Rubeola
Rubella
rhabdovirus
Rabies
Human vaccine
– Human diploid cell
– DEV- Duck’s embryo vaccine
Animal vaccine
– Flurry stain
– Street Alabama dufferin strain
Heller stain
Negri bodies
Rabies
Virus enters through bite, grows at
trauma site for a week and multiplies,
then enters nerve endings and
advances toward the ganglia, spinal
cord and brain.
Infection cycle completed when virus
replicates in the salivary glands
63
Clinical phases of
rabies:
Prodromal phase – fever, nausea, vomiting,
headache, fatigue; some experience pain,
burning, tingling sensations at site of
wound
Furious phase – agitation, disorientation,
seizures, twitching, hydrophobia
Dumb phase – paralyzed, disoriented,
stuporous
Progress to coma phase, resulting in death
65
DNA VIRUS
Adenovirus
Pox virus
Herpes virus
Human papova virus
Hepatitis virus
Adenovirus
Tonsilitis
Adenitis
Mild respiratory illness
Coryza
cough
ADENOVIRUS
Pox virus
Small pox ( variola major )
Alastrim ( variola minor )
SMALL POX
Herpes virus
Herpes simple type A
– Gingivomastitis
– Vesicular eruption of the membrane
of oral cavity
Herpes simplex type B
– Vulvovaginitis
– Danger of congenital complication
( liver, CNS)
Genital Herpes
Transmission
Major routes: sexual & mother-to-infant
Most sexual transmission probably occurs
when index case is asymptomatic
Efficiency of transmission is greater from
men to women than women to men
u Mertz, et al: 144 serodiscordant couples
u Almost 17% man-to-woman transmission
u Almost 4% woman-to-man transmission
Male Female Herpes
Herpes
Genital Herpes
Condom Effectiveness
Latex condoms, when used
consistently and correctly, are highly
effective for:
– HIV
And can reduce the risk of:
– GC, CT, and Trichomonas
– Genital herpes, syphilis, chancroid, and
HPV, only when the infected areas are
covered by the condom
CDC, 2002
GENITAL HERPES
GENITAL HERPES
Genital Herpes (HSV)
Transmission: skin to skin
Symptoms:
Prodrome--tingling in legs, buttocks or groin
Lesion--itching, blister at infection site;
Recurrences vary in frequency and severity
Time to onset: 2-20 days
Pregnancy: 5% transmission when lesions present
Diagnosis: culture, antibody test
Treatment: symptom relief; antivirals effective
Herpes of the Newborn
HSV-1 and HSV-2
Potentially fatal in the neonate and
fetus
Infant contaminated by mother
before or during birth; hand
transmission by mother to infant
Infection of mouth, skin, eyes, CNS
Preventative screening of pregnant
women; delivery by C-section if
outbreak at the time of birth
83
HERPES LABIALIS
Varicella
– Virus of chicken pox
– Might lead pneumonitis and
encephalitis
– Herpes zoster
VARICELLA - ZOSTER
CHICKENPOX /
SHINGLES
CMV
– Inclusion mononucleosis
– Liver, kidney and lungs
– Associated with mild hepatitis
– Recognized in congenital condition
– Oncogenic potential
CMV CHILD INFECTION
EBV
– Infectious mononucleosis
– Agent of Burkitt’s lymphoma
– Nasopharyngeal carcinoma
– Oncogenic virus
HHV5 EPSTEIN BARR VIRUS
causes INFECTIOUS
MONONUCLEOSIS &
BURKITT’S LYMPHOMA
HUMAN PAPOVA VIRUS
Papilloma virus
– Verruca vulgaris
– Condylomata acuminata
Polyoma virus
– JV virus ( progressive multifocal
leucoencephalopathy )
– BK virus ( kidney transplant, chronic
disease )
Papilloma virus
Verruca vulgaris
Condylomata acuminata
Typical Genital Warts
Sharps/needle sticks
HBV Cannot be Spread
by:
Sneezing or
coughing
Kissing or hugging
Breast feeding
Food or water
Sharing eating
utensils or drinking
glasses
Casual contact
121
HIV-1 and HIV-2
T-cell lymphotropic viruses I and
II – leukemia and lymphoma
HIV can only infect host cells
that have the required CD4
marker plus a coreceptor.
Legend
Th- T- helper
MCH- major histocompatibility
complex
CTL- cytotoxic T cell
Cells of the immune
system ( review )
B- cells
– Plasma cells
– Memory cells
T- cells
Helper T cells (effector T cells or Th cells)
are the "middlemen" of the
adaptive immune system. Once activated,
they divide rapidly and secrete small
proteins called cytokines that regulate or
assist in the immune response. Depending
on the size, cytokine signals received, these
cells differentiate into TH1, TH2, TH3, TH17,
THF, or one of other subsets, which secrete
different cytokines. CD4+ cells are
associated with MHC class II.
About T-helper
T helper cells (also known as
effector T cells or Th cells) are
a sub-group of lymphocytes (a
type of white blood cell or
leukocyte) that play an important
role in establishing and
maximizing the capabilities of the
immune system.
they have no cytotoxic or
phagocytic activity; they cannot
kill infected host (also known as
somatic) cells or pathogens,
Th cells are involved in activating
and directing other immune cells,
and are particularly important in
the immune system
Mature Th cells are believed to
always express the surface
protein CD4. T cells expressing
CD4 are also known as CD4+ T
cells.
Cytotoxic T cells (TC cells, or CTLs) destroy virally
infected cells and tumor cells, and are also implicated in
transplant rejection. These cells are also known as CD8+
T cells (associated with MHC class I), since they express
the CD8 glycoprotein at their surface. Through SLOB[
clarification needed] interaction with T regulatory
CD4+CD25+FoxP3+ cells, these cells can be inactivated
to a anergic state, which prevent autoimmune diseases
such as experimental autoimmune encephalomyelitis.[1]
Memory T cells are a subset of antigen-specific T
cells that persist long-term after an infection has
resolved. They quickly expand to large numbers of
effector T cells upon re-exposure to their cognate
antigen, thus providing the immune system with
"memory" against past infections. Memory T cells
comprise two subtypes: central memory T cells (TCM
cells) and effector memory T cells (TEM cells).
Memory cells may be either CD4+ or CD8+.
Regulatory T cells (Treg cells), formerly known as
suppressor T cells, are crucial for the maintenance of
immunological tolerance. Their major role is to shut down T
cell-mediated immunity toward the end of an immune
reaction and to suppress auto-reactive T cells that escaped
the process of negative selection in the thymus. Two major
classes of CD4+ regulatory T cells have been described,
including the naturally occurring Treg cells and the adaptive
Treg cells. Naturally occurring Treg cells (also known as
CD4+CD25+FoxP3+ Treg cells) arise in the thymus, whereas
the adaptive Treg cells (also known as Tr1 cells or Th3 cells)
may originate during a normal immune response. Naturally
occurring Treg cells can be distinguished from other T cells
by the presence of an intracellular molecule called FoxP3.
Mutations of the FOXP3 gene can prevent regulatory T cell
development, causing the fatal autoimmune disease
Natural killer T cells (NKT cells) are a special
kind of lymphocyte that bridges the
adaptive immune system with the
innate immune system. Unlike conventional T
cells that recognize peptide antigen presented by
major histocompatibility complex (MHC)
molecules, NKT cells recognize glycolipid antigen
presented by a molecule called CD1d. Once
activated, these cells can perform functions
ascribed to both Th and Tc cells (i.e., cytokine
production and release of cytolytic/cell killing
molecules).
γδ T cells (gamma delta T cells) represent a small
subset of T cells that possess a distinct T cell receptor
(TCR) on their surface. A majority of T cells have a TCR
composed of two glycoprotein chains called α- and β- TCR
chains. However, in γδ T cells, the TCR is made up of one
γ-chain and one δ-chain. This group of T cells is much less
common (5% of total T cells) than the αβ T cells, but are
found at their highest abundance in the gut mucosa,
within a population of lymphocytes known as
intraepithelial lymphocytes (IELs). The antigenic
molecules that activate γδ T cells are still widely
unknown. However, γδ T cells are not MHC restricted and
seem to be able to recognise whole proteins rather than
requiring peptides to be presented by MHC molecules on
antigen presenting cells.
HIV and AIDS
The Cellular Picture
of one cell type throughout the course of the d
CD4+ T4 helper cells
A fall in the CD4+ cells always precedes diseas
In advanced disease: the loss of
another cell type
CD8+ cytotoxic killer cells
Suggests an infectious agent
A virus
But initially difficult to grow
Rapidly kills cells on which it grows
AIDS
Definition
• AIDS is currently defined as the
presence of one of 25 conditions
indicative of severe immunosuppression
OR
• HIV infection in an individual with a
CD4+ cell count of <200 cells per cubic
mm of blood
• AIDS is therefore the end point of an
infection that is continuous, progressive
and pathogenic
143
Men account for 70% of new
infections.
Anal sex provides an entrance for
the virus.
IV drug abusers can be HIV carriers;
significant factor in spread to
heterosexual population
Insert figure 25.14
HIV routes of infection
145
Pathogenesis and Virulence
Factors of HIV
HIV enters through mucous
membrane or skin and travels to
dendritic phagocytes beneath the
epithelium, multiplies and is shed.
Virus is taken up and amplified by
macrophages in the skin, lymph
organs, bone marrow, and blood.
HIV attaches to CD4 and
coreceptor; HIV fuses with cell
membrane.
146
Reverse transcriptase makes a
DNA copy of RNA.
Viral DNA is integrated into host
chromosome (provirus).
Can produce a lytic infection or
remain latent
Inexorable decline of
CD4+ T4 cells
Why do all
of the T4
cells
disappear
?
At early
stages of
infection
only 1 in
10,000
cells is
infected
Late 1 in
Of great importance to therapeutic strategy
40
Virus destroys the cell as
a result of budding
Why do
all T4
1.
PUNCTURED cells
Why do all T4 cells
disappear? - 2
But
syncytia
not
Infected CD4
cell Cells Fuse common
G protein
CXCR4
signal
? chemokin
e receptor
?
Binding to
Binding to
CXCR4 results
CXCR4 results in in expression of
expression of TNF-alpha on
TNF-alpha the cell surface
Why do all T4 cells
disappear?
Induction of apoptosis
CD8 cell
CXCR4
Macrophage
Death
CD8 T cell
apoptotic
bodies
Macrophages may be
infected by two routes
HIV gp1
20 CD
4 HIV gp120 binds to
macrophage CD4
antigen
Virus is opsonized
by anti gp120
antibodies which
bind to
Fc macrophage Fc
recepto receptors - an
r
Anti- enhancingproblem
vaccine
gp120 antibody
HIV
Primary effects of HIV infection:
– extreme leukopenia – lymphocytes in particular
– formation of giant T cells and other syncytia allowing
the virus to spread directly from cell to cell
– Infected macrophages release the virus in central
nervous system, with toxic effect, inflammation.
Secondary effects of HIV:
– Destruction on CD4 lymphocytes allows for
opportunistic infections and malignancies.
156
Signs and Symptoms of HIV
Infections and AIDS
Symptoms of HIV are directly related
to viral blood level and level of T
cells.
Initial infection – mononucleosis-like
symptoms that soon disappear
Asymptomatic phase 2-15 years
(avg. 10)
157
Antibodies are detectable 8-16 weeks
after infection.
HIV destroys the immune system.
When T4 cell levels fall below 200/µ L
AIDS symptoms appear including fever,
swollen lymph nodes, diarrhea, weight
loss, neurological symptoms,
opportunistic infections and cancers.
Diagnosis of HIV
Infection
Testing based on detection of
antibodies specific to the virus in
serum or other fluids; done at 2
levels
Initial screening
159
Follow up with Western blot
analysis to rule out false positives
False negatives can also occur;
persons who may have been
exposed should be tested a
second time 3-6 months later.
Insert Table 25.A page 776
AIDS-defining illnesses
161
Preventing and Treating
HIV
No vaccine available
– monogamous sexual relationships
– condoms
– universal precautions
162
No cure; therapies slow down the
progress of the disease or diminish
the symptoms
– inhibit viral enzymes: reverse
transcriptase, protease, integrase
– inhibit fusion
– inhibit viral translation
– highly active anti-retroviral therapy
HIV