VIROLOGY

 Viruses are the smallest infectious

agents (20-300 nanometers)
 Possess only one kind of nucleic acid,
either DNA or RNA as their genome
 Capable of replication only within living
cells (genetic parasites)
3
Viral Structure
 General Structure of
5
Viruses
 Size range –
– most <0.2 μm; requires electron
microscope
 Virion – fully formed virus able to
establish an infection
 Prions - misfolded proteins, contain no nucleic
acid
– cause transmissible spongiform encephalopathies –
fatal neurodegenerative diseases
– common in animals:
 scrapie in sheep & goats
 bovine spongiform encephalopathies (BSE), aka mad cow
disease
 wasting disease
 humans – Creutzfeldt-Jakob Syndrome (CJS)
 Extremely resistant to usual sterilization
techniques
 Other noncellular
7
infectious agents
 Satellite viruses – dependent on
other viruses for replication
– adeno-associated virus – replicate only in
cells infected with adenovirus
– delta agent – naked strand of RNA
expressed only in the presence of
hepatitis B virus
 Viroids - short pieces of RNA, no
protein coat; only been identified in
plants, so far
Viral Structure:
Covering
 FUNCTIONS:
– Protects the nuclear material
– Responsible for introduction of viral
nucleic acid into a suitable host cell
– Stimulates the immune system
Viral Structure:
Covering - CAPSID
 CAPSID: The outer protective shell
– The most prominent geometric feature
– Composed of identical protein subunits
– CAPSOMERS
– Formed by spontaneous self-assembly
of capsomers
Viral Structure: Naked
Viruses
Viral Structure: Covering
- ENVELOPE
 Formed when the viral particle carries off
a part of the host cell’s membrane (any
part of the endomembrane system may
be used)
 SPIKES or PEPLOMERS
– Protein spikes protruding through the envelope
from the capsid
– Essential for attachment to the next host
Viral Structure:
Enveloped Viruses
 Viral Structure: Central
Core – Nucleic Acids
 Genetic material of
the particle
 Viruses may contain
either DNA or RNA
BUT NOT BOTH
 DNA or RNA may exist
as single or double-
stranded
Viral Morphology

Helical Icosahedral
Viral Morphology

Enveloped Complex
Modes of Viral Multiplication

 Adsorption - binding of virus to specific

molecule on host cell
 Penetration - genome enters host cell
 Uncoating – the viral nucleic acid is released
from the capsid
 Synthesis – viral components are produced
 Assembly – new viral particles are constructed
 Release – assembled viruses are released by
budding (exocytosis) or cell lysis
 Release
17
 budding – exocytosis; nucleocapsid binds
to membrane which pinches off and sheds
the viruses gradually; cell is not
immediately destroyed
 lysis – nonenveloped and complex viruses
released when cell dies and ruptures
 Number of viruses released is variable
– 3,000-4,000 released by poxvirus
– >100,000 released by poliovirus
Cytopathic effects - virus-induced
damage to cells

 Changes in size & shape

 Cytoplasmic inclusion bodies
 Nuclear inclusion bodies
 Cells fuse to form multinucleated cells.
 Cell lysis
 Alter DNA
 Transform cells into cancerous cells
19
Persistent Infections
 Persistent infections - cell harbors the virus and
is not immediately lysed
 Can last weeks or host’s lifetime; several can
periodically reactivate – chronic latent state
– measles virus – may remain hidden in brain cells for
many years
– herpes simplex virus – cold sores and genital herpes
– herpes zoster virus – chickenpox and shingles
20
 Some animal viruses enter host cell and permanently
alter its genetic material resulting in cancer –
transformation of the cell.
 Transformed cells have increased rate of growth,
alterations in chromosomes, and capacity to divide
for indefinite time periods resulting in tumors.
 Mammalian viruses capable of initiating tumors are
called oncoviruses.
– Papillomavirus – cervical cancer
– Epstein-Barr virus – Burkitt’s lymphoma
22
Lysogeny
 Lysogeny results in the spread of the
virus without killing the host cell.
 Phage genes in the bacterial
chromosome can cause the production
of toxins or enzymes that cause
pathology – lysogenic conversion.
– Corynebacterium diphtheriae
– Vibrio cholerae
– Clostridium botulinum
Lysogeny
Modes of entry
 Respiratory tract though
inhalation
 Gastrointestinal tract
 Skin
 Sexual
 Direct contact
 Transfusion of blood
Effects of virus on the
host cell
 CPE or cellular effect
 Transformation of normal cell to
malignant cell
 Latent infection
 Clumping of RBC
Some of the Medically
Important Viruses
Family Genus Common Disease
Name of
Genus
Members
DNA Viruses
Herpesviridae Simplexvirus Herpes simplex Cold sores,
1&2 virus genital herpes

Varicella zoster Chicken pox

virus
Adenoviridae Mastadenoviru Human Colds, URI
s adenovirus
Papovaviridae Papillomavirus Human Warts
papillomavirus
(HPV)
 Some of the Medically
Important Viruses
Family Genus Common Disease
Name of
Genus
Members
RNA Viruses
Picornaviridae Enterovirus Poliovirus Poliomyelitis
Hepatovirus Hepatitis A virus Short-term
hepatitis
Rhinovirus Human Common colds
rhinovirus
Togaviridae Alphavirus Rubella virus German
measles
Flaviviridae Flavivirus Dengue fever Dengue fever
virus
Filoviridae Filovirus Ebola virus Ebola fever
RNA VIRUS
 Picornavirus
– Entero virus
 Arbo virus
– Alpha
– Flavi virus
 Myxo virus
– Paramyxovirus
– Orthomyxovirus
– pseudomyxovirus
 Rhabdo virus
Picorna virus

– Smallest RNA virus

– Single strand RNA
ENTEROVIRUS

 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

 Fever, body aches, and malaise

 May or may not experience respiratory symptoms with

breathing problems; severe cases can result in
respiratory distress and death
 Diagnosis relies on exclusion of other likely agents.

 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

DOIA Website, 2000

Male HPV infection
Female HPV
Polyoma virus
The ABC’s of Hepatitis

US&A (v. 2/07) 109

HBV - Hepatitis
HBV Transmission
B
 Unprotected sex with
multiple partners

 Sharing needles during

injecting drug use

 From infected mother

to child during birth

 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

US&A (v. 2/07) 111

 Hepatitis B
 Hepatitis B virus (HBV) is 100 more
infectious than HIV
 About 5% of Americans have been
infected with HBV at some point
during their lifetime
 People who get infected with HBV
can also get infected with Hepatitis D
virus (HDV). If this happens, people
often become very sick
US&A
(v.
2/07)
 HCV - Hepatitis C
Clinical Features
Incubation period Average 6-7 weeks
Range 2-26 weeks
No sign or symptoms 80%
Acute illness (jaundice) ≤ 20% (Mild)
Chronic infection Age- 75%-85%
Chronic liver diseaserelated 10%-70% (most are
asymptomatic)
Deaths from chronic liver 1%-5%
disease
Immunity No protection from future
infection identified
 HCV
Symptoms
- Hepatitis C
• flu-like symptoms
• jaundice
• fatigue
• dark urine
• abdominal pain
• loss of appetite
• nausea
HCV Transmission

• Injecting drug use

• Hemodialysis (long-term)
• Blood transfusion and/or
organ transplant before
1992
• From infected mother to
child during birth
• Occupational exposure to
blood - mostly
needlesticks
• Sexual or household
exposures - rare
Sources of Infection --
Hepatitis C

US&A (v. 2/07) 116

 Hepatitis C
 Risk Factors:
– Long-term kidney
dialysis
– Sex with multiple
partners
– Tattooing or body
piercing with
shared needles or
unsterilized
equipment
– Intranasal cocaine
use with shared
straws
Pamela Anderson claims her infection came from a
tattoo needle
Etiology of HIV
 HTLV-III- Human T cell
Lymphotrophic virus III
 LAV- lymphadenopathy-
associated virus
 * contains single RNA strand and
a DNA synthesizing enzyme
called reverse transcriptase
 Causative Agent
 Retrovirus, genus Lentivirus
 Encode reverse transcriptase enzyme
which makes a double stranded DNA
from the single-stranded RNA genome
 Viral genes permanently integrated
into host DNA
 Human Immunodeficiency Virus (HIV)
the cause of Acquired
Immunodeficiency Syndrome (AIDS)

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

• With the prevalence of HIV in the

developing world, HIV and its
 HIV and AIDS
The cellular and
immunological picture
The course of the disease
• High 1. Acute
virus titer Infection
• Mild symptoms
• Fall in CD4+ cells but recovers
• Rise in CD8+ cells but recovers
• A high virus titer (up to 10 million
viruses per ml blood)
• Macrophages
Macrophages infected
bring HIV into the body if sexually transmitted
HIV and AIDS
2. A strong immune response

Virus almost disappears from

circulation
• Good cytoxic T cell response
• Soluble antibodies appear later
against both surface and internal
proteins
• Most virus at this stage comes
from recently activated (dividing)
and infected CD4+ cells
•
 HIV and AIDS
3. A latent state

Latency of virus and of

symptoms
• Virus persists in extra-
vascular tissues
• Lymph node dendritic
cells
• Resting CD4+ memory
cells (last a very
long time - a very stable
 HIV and AIDS

• 10 billion HIV particles per day

• Virus half life 5.7 hours
• 100-10 million virions per ml blood
(set point)
• Small minority of T4 cells are
infected
• Virus found in lymph nodes
 HIV and AIDS
4. The beginning of disease
Massive loss of CD4+ cells
• CD4+ cells are the targets of the virus
• Cells that proliferate to respond to the
virus are killed by it
• Dendritic cells present antigen and virus
to CD4 cells
• Epitope variation allows more and more
HIV to
escape from immune response just as
response wanes
• Apoptosis of CD4+ cells
 HIV and AIDS
Advanced disease - AIDS
CD8+ cells destroy more
CD4+ cells
• CD4 cell loss means virus and
infected
cells no longer controlled
• As CD4+ cells fall below 200
per cu mm
virus titer rises rapidly and
remaining immune response
collapses
• CD8+ cell number collapses
• Opportunistic infections
Epidemiology of HIV
Infections
 Transmission occurs by direct and
specific routes: mainly through
sexual intercourse and transfer of
blood or blood products; babies can
be infected before or during birth,
and from breast feeding.
 HIV does not survive long outside of
the body.

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

But few cells are infected:

Early stage of infection
1:10,000
Late 1:40

Why do
all T4
1.
PUNCTURED cells
 Why do all T4 cells
disappear? - 2
But
syncytia
not
Infected CD4
cell Cells Fuse common

Gp120 positive Most T4

cells are
not HIV+
Could
Uninfected “sweep up”
Killing of CD4 cells CD4 cell
uninfected
2. Syncytium Gp120 cells
Formation negative
 Why do
all T4
cells
disappea
r?
Cytotoxi
c T cell

Killing of CD4 cells

3. Cytotoxic T cell-mediated
lysis
BUT: Most cells
are not infected
Killing of CD4+ cells
4. Binding of free
Gp120 to CD4
antigen makes
uninfected T4
cell look like an
infected cell
Complement-
mediated lysis
Could account
for the loss of
uninfected T4
cells
 Why do all T4 cells
disappear?
Induction of apoptosis
CD8 cell gp120
Macrophage
(no CD4 antigen)
HIV
chemokine

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.

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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)

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 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

– ELISA, latex agglutination and rapid

antibody tests
– rapid results but may result in false
positives

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 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

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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