Microbiology, virology, immunology
department
DNA-VIRUSES:
HERPESVIRUSES.
ADENOVIRUSES
RETROVIRUSES. AIDS.
ONCOGENIC VIRUSES.
PRIONS.
Family Herpesviridae
Morphology
# icosahedral capsid (100 nm)
# 162 capsomers
# envelope(150-250 nm)
# genome:linear double stranded DNA
Replication
nucleus
budding through nuclear membrane
Herpesvirus Subfamily
Alphaherpesvirinae
Betaherpesvirinae
Gammaherpesvirinae
Herpesviridae

Alphaherpesvirinae (ectodermal tissue
tropism)



Betaherpesvirinae




Grow rapidly
Latency in sensory neurons
Cytomegaloviruses (large balloon-like cells)
Grow slowly
Latency in salivary glands, kidneys, lymphocytes
Gammaherpesvirinae (malignant catarrhal fever
virus)
 Lymphoproliferative diseases
 Latency in lymphoid cells
Human Herpesviruses (HHV)
HHV-1 - > Herpes simplex virus 1
HHV-2 - > Herpes simplex virus 2
HHV-3 - > Varicella-zoster virus
HHV-4 - > Epstein-Barr virus
HHV-5 - > Cytomegalovirus
HHV-6 - >HumanB cell lymphotropic virus
HHV-7 - > isolated from CD4+ cell
HHV-8 - > Kaposi’sarcoma associated
herpesvirus (KSHV)
Herpes simplex virus (HSV)
Properties
 ectodermal tissue tropism
 vesicle lesion
 infection - > multinucleated cell
 latency
• HSV-1- > trigerminal nerve ganglia
• HSV-2- > lumbosacral nerve ganglia
recurrent infection stimuli:
stress,fever,sun light,drugs
Cytopathic effect (right)
(infected cells develop intranuclear acidophilic
inclusion and then undergo necrosis )
HERPES SIMPLEX:
Human Herpesvirus 1 (Herpes Labialis) &
Human Herpesvirus 2 (Herpes Genitalis).
Infection with herpes simplex virus may take
several clinical forms. The infection is most often
inapparent. The usual clinical manifestation is a
vesicular eruption of the skin or mucous
membranes. Infection is sometimes seen as severe
keratitis, meningoencephalitis, and a disseminated
illness of the newborn.
HSV-1 life cycle:
Primary infection.
1. Productive
Infection
HSV life cycle:
Establishment of latency.
1. Productive
Infection
2. Establishment
of latency
HSV life cycle:
reactivation of latent virus.
Common
triggers:
- sunburn
- fever
- “exam stress”
3. Reactivation
of latent virus
HSV life cycle:recurrent
disease and viral shedding.
4. Cold sores.
Virus spread
to new host.
3. Reactivation
of latent virus
Herpes labialis
(cold sores, herpes febrilis).
This is the most common recurrent
disease produced by type 1.
The vesicle ruptures, leaving a painful
ulcer that heals without scarring. The
lesions may recur, repeatedly and at
various intervals of time, in the same
location.
The permanent site of latent herpes
simplex virus is the trigeminal ganglion.
Herpes labialis
Usually
cold sores occur along
the mucocutaneous junction of
the lips.
They may be single or
clustered.
They may develop following
stress or another trigger or
without an apparent stimulus.
The duration is usually 10-14
days.
Treatment is usually necessary
only in immune-compromised
patients.
Herpes labialis
Recurrent herpes infections can affect
other parts of the body.
Keratoconjunctivitis.
The initial infection with herpesvirus may
be in the eye, producing severe
keratoconjunctivitis. Recurrent lesions of
the eye appear as dendritic keratitis or
corneal ulcers or as vesicles on the eyelids.
With recurrent keratitis, there may be
progressive involvement of the corneal
stroma, with permanent opacification and
blindness.
Genital herpes (herpes progenitalis).
Genital herpes is characterized by
vesiculoulcerative lesions of the penis of the
male or the cervix, vulva, vagina, and
perineum of the female. The lesions are
more severe during primary infection and
may be associated with fever, malaise, and
inguinal lymphadenopathy.
Type 2 virus remains latent in lumbar and
sacral ganglia.
Natural history
1. Start as vesicles
2. Ulcer formation
Severe HSV Outbreaks
Neonatal infections
Usually these are due to HSV-2.
Herpesvirus type 2 may be
transmitted to the newborn during
birth by contact with herpetic lesions
in the birth canal. Approximately half
of the children born to mothers with
active lesions will be infected.
Neonatal infections
The spectrum of illness produced in the
newborn appears to vary from subclinical or
local to severe generalized disease with a fatal
outcome.
Clinical syndromes include:
 Encephalitis
 Disseminated multi-organ infection
(liver, spleen, lungs)
Diagnosis of Herpes simplex
virus infections
 Clinical
syndrome
recognition
 Electron
microscopy
 Virus isolation
 Viral serology is
generally not
useful
Laboratory Diagnosis
The virus may be isolated from herpetic lesions
(skin, cornea, or brain).
The appearance of typical cytopathic effects in cell
culture suggests the presence of herpesvirus in 1836 hours. Scrapings or swabs from the base of early
herpetic lesions contain multinucleated giant cells.
Serology: The agent is then identified by
neutralization test or immunofluorescence staining
with specific antiserum. Antibodies appear in 4-7
days; can be measured by NT, IHT, CFT, RIA and
reach a peak in 2-4 weeks.
HV, immune fluorescence test
Tzanck Test
A smear of an opened skin vesicle to detect
multinucleated giant cells.
Used to assay for HSV-1, HSV-2, and VZV.
Tzanck heavens I
do not have herpes!
Treatment of HSV infections

In normal hosts treatment provides only a 1-2 day
benefit for cold sores

Acute primary genital infections may be treated with
acyclovir or a “cousin”.

Recurrent genital infection can be prevented with
the use of long term prophylactic acyclovir.

Acyclovir can also be used to treat serious
infections in severely immuno-compromised
patients and in brain or systemic infections.
VARICELLA-ZOSTER VIRUS (VZV)
(Human Herpesvirus 3 – HHV-3)
Varicella (chickenpox) is a mild, highly
infectious disease, chiefly of children,
characterized clinically by a vesicular eruption of
the skin and mucous membranes. The causative
agent is indistinguishable from the virus of zoster.
Zoster (shingles) is a sporadic, incapacitating
disease of adults (rare in children) that is
characterized by an inflammatory reaction of the
posterior nerve roots and ganglia, accompanied by
crops of vesicles (like those of varicella) over the
skin supplied by the affected sensory nerves.
VARICELLA-ZOSTER VIRUS
(Human Herpesvirus 3)
(Chickenpox, Herpes Zoster,
Shingles, Zona)
Both diseases are caused by
the same virus.
Varicella is the acute disease that follows
primary contact with the virus,
whereas zoster is the response of the
partially immune host to a reactivation of
varicella virus present in latent form in
sensory ganglia.
Chickenpox Transmission
 Persons
to person
contact or
sneezing/coughing
 Kids around 6 or 7
will usually spread
it between each
other.
Pathogenesis & Pathology
of Varicella:
The route of infection is probably the
mucosa of the upper respiratory tract. The
virus probably circulates in the blood and
localizes in the skin. Swelling of epithelial
cells, ballooning degeneration, and the
accumulation of tissue fluids result in vesicle
formation. In nuclei of infected cells,
particularly in the early stages, eosinophilic
inclusion bodies are found.
Varicella virus, pathogenesis
Characterized by:
Fever
Raw, open, itchy sores
Varicella
Chickenpox
Complications
 Bacterial
Infections
 Viral Pneumonia
 Bleeding Problems
 Infection of the brain
Treatment
 Acyclovir
 Tylenol
 In
medieval times and still
today, oatmeal baths are used
to relieve itching.
Prevention
Vaccination(Varicella)
A live attenuated vaccine is available.
• Quarantine
Or…for the extremely
paranoid
• Kill everyone around you
Pathogenesis & Pathology.
In addition to skin lesions —
histopathologically identical with those of
varicella — there is an inflammatory reaction of
the dorsal nerve roots and sensory 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. There is cellular
infiltration, necrosis of nerve cells, and
inflammation of the ganglion sheath.
Zoster:
Shingles
 If
you come in contact with someone
with Shingles and you haven’t had
Chicken Pox yet, you will get Chicken
Pox and not Shingles
 There is no vaccine for Shingles.
There is work being done to create
one. It is expected to take about 5
years
Zoster
Shingles
CYTOMECALOVIRUS
(Human Herpesvirus 5)

Asymptomatic in normal humans, acquired as
adult; also produces cytomegalic inclusion
disease in newborn; also non-heterophile
transfusion mononucleosis; problem in
immunocompromised

high degree of shedding in pregnancy

may be an STD

Retinitis, and detached retina in 25%

treated with ganciclovir in severe cases
Clinical Manifestations.
Cytomegalovirus infection can result in one
of three distinct clinical syndromes.
Congenital cytomegalovirus infection:
hepatospleno-megaly, retinitis, a
petechial/purpuric skin rash, and
involvement of the central nervous system
(ventriculo-megaly, intracranial
calcifications, etc).
Clinical Manifestations.
Mononucleosis syndrome (fever, malaise,
atypical lymphocytosis, pharyngitis and,
rarely, cervical adenopathy or hepatitis)
Third clinical entity is cytomegalovirus
infection in severely
immunocompromised individuals. In
these patients, infection can involve the
lungs, gastrointestinal tract, liver, retina, and
central nervous system
Persistence of CMV
common;
10-15% in teens;
50% by age 35
part of the differential for hepatitis
Virus isolated from urine, blood, throat
washings, saliva, tears, breast milk,
semen, stool, amniotic fluid, cervical
secretions and tissue for transplantation
(now tested)
Cytopathic Effect of VZV
Cytopathic Effect of VZV in cell culture: Note the
ballooning of cells. (Coutesy of Linda Stannard, University of Cape Town,
S.A.)
Cytomegalovirus Inclusion Diseases.
Electron micrograph of a single animal
cell infected with the cytomegalovirus.
The intranuclear inclusion body has
a typical” owl-eyed” apearence.
Pathogenesis.
Cytomegalovirus can cause persistent infection
in various tissues, including those of the salivary
glands, breasts, kidneys, endocervix, seminal
vesicles and peripheral blood leukocytes. This
persistent infection leads to chronic viral excretion
by the involved organ. Transmission of virus is
through contact with infected secretions. The
average incubation period is four to six weeks.
It should also be noted that the kidneys of organ
donors can be a source of cytomegalovirus for the
recipient, and that peripheral blood leukocytes
have been implicated in the transmission of
cytomegalovirus via blood transfusion.
Epstein-Barr virus
 The
usual source of infection is the saliva
of persons shedding the virus.
 The virus has an affinity for receptors on
the surface of B cells.
 Viral infection results in local replication
and a secondary viremia. There is
proliferation of both B cells and the T8
(suppressor) subset of T cells.
EB HERPESVIRUS
(Human Herpesvirus 4).
EB (Epstein-Barr) virus is
the
causative
agent
of
infectious mononucleosis and
has been associated with
Burkitt's
lymphoma
and
nasopharyngeal carcinoma.
Epidemiology. Epstein-Barr virus is transmitted by
intimate contact.
Pathogenesis. Epstein-Barr virus is tropic for Blymphocytes.
Mononucleosis
Characterized by fever,
hepatosplenomegaly, pharyngitis, and
lymphadenopathy (especially posterior
auricular nodes)
Peak incidence 15-20 years old.
Abnormal circulating cytotoxic T cells
(atypical lymphocytes).
Most common during peak
kissing years (“kissing disease”)
Clinical manifestations
of EBV infections
Infectious mononucleosis
The incubation period is 4-6 weeks.
The illness may last from 2-8 weeks.
Fatigue may persist for months
Clinical manifestations
of EBV infections
Infectious mononucleosis
Symptoms and signs
 tonsilar enlargement
 pharyngeal redness with or without pus
 cervical adenopathy (80-90%)
 large liver and spleen
 skin rash, esp. after ampicillin
Diagnosis of EBV infection
 Increased
lymphocytes and
monocytes
 Atypical lymphocytes (usually >30%)
 Neutropenia (low neutophils) and
thrombocytopenia (low platelets)
 Most have elevated liver enzymes
 Other specific serologic tests
directed against viral antigens
Atypical
lymphocytes
Typical
pharyngitis
Treatment of EBV infections
Treatment is usually supportive
Infectious
mononucleosis
Nasopharyngeal
carcinoma
Burkitt’s Lymphoma (1)

Burkitt's lymphoma (BL) occurs endemically in parts
of Africa (where it is the commonest childhood
tumour) and Papua New Guinea. It usually occurs
in children aged 3-14 years. It respond favorably to
chemotherapy.

It is restricted to areas with holoendemic malaria.
Therefore it appears that malaria infection is a
cofactor.

Multiple copies of EBV genome and some EBV
antigens can be found in BL cells and patients with
BL have high titres of antibodies against various
EBV antigens.
Burkitt's lymphoma
Oncogenic Properties:
Herpesviruses have been linked with
malignant diseases in humans :
herpes simplex virus type 2 with cervical and
vulvar carcinoma;
EB virus with Burkilt 's lymphoma of African
children and with nasopharyngeal carcinoma.
Other Herpesviruses
HHV-6 - Roseola or exanthem subitum
so-called “sixth” exanthem
 HHV-7 - T lymphotropic and produces rashlike illness
 HHV-8 - associated
with Kaposi’s sarcoma
in AIDS patients

DREAMS
CAME
TRUE?
Adenoviruses (ADV)
a group of viruses that infect the membranes
(tissue linings) of the respiratory tract, the eyes, the
intestines, and the urinary tract.


first isolated from adenoidal tissue in 1953.
Family
Genus
Adenoviridae
Mastadenovirus
Adenoviruses are double-stranded
DNA viruses. They have icosahedral
capsids with twelve vertices and
seven surface proteins. The virion is
non-enveloped, spherical and about
seventy to ninety nm in size.
ADENOVIRUS - Classification
Subgroups- 6 subgroups (A-F), based
on hemagglutination
Serotypes- 1-49 (human)
Common serotypes:- 1-8, 11, 21, 35,
37, 40
Enteric Adenoviruses belong to
subgroup F
Transmission
Ingestion/Fecal-Oral Route
Respiration (through respiratory
droplets)
Contact/Hand-to-eye transfer
Venereal
The types of adenovirus that cause respiratory
and intestinal infections spread from person to
person through respiratory secretions (coughs or
sneezes) or fecal contamination. Fecal material
can be ingested through contamination of water
supplies, eating food contaminated by houseflies,
or poor hygiene after handling diapers.
Indirect transmission can occur through
exposure to the contaminated surfaces of furniture
and other objects.
The types of adenovirus causing conjunctivitis
may be transmitted by water (in lakes and
swimming pools), by sharing contaminated objects
(such as towels or toys), or by touch.
Adenoviral infections
affect infants and young children much more frequently
than adults.
Signs and Symptoms
Depending on which part of the body is affected,
the signs and symptoms of adenoviral infections
vary:
 Febrile respiratory disease: bronchiolitis, croup,
pneumonia
 Gastroenteritis
 Urinary tract infection: cervicitis, urethritis,
hemorrhagic cystitis
 Eye Infections: Conjunctivitis, Keratoconjunctivitis
Adenoviral infections
Most adenoviral infections last from a
few days to a week.
Severe respiratory infections may
last longer and cause lingering
symptoms, such as a cough.
Pneumonia can last anywhere from 2 to
4 weeks.
Laboratory Diagnosis.
The viruses have been isolated
→ from throat swabs,
→ conjunctival swabs,
→ rectal swabs, stools of patients,
→ urine,
→ from the eye (from patients with
conjunctivitis).
Laboratory Diagnosis.
The viruses are isolated by
inoculation of tissue cultures of human
cells in which characteristic cytopathic
changes are produced.
A new serotype that has not been
isolated in cell cultures can be detected
by direct examination of fecal extracts
by electron microscopy or by enzymelinked immunosorbent assay.
Serology. In most cases, the neutralizing
antibody titer of infected persons shows a
4-fold or greater rise against the type
recovered from the patient in NT.
The CF test, using the common antigen,
is an easily applied method for detecting
infection by any member of the group.
A sensitive radioimmunoassay can
measure serum antibody to type 5 fiber
antigen.
Treatment
Adenoviral illnesses often resemble
certain bacterial infections, which can be
treated with antibiotics.
But antibiotics don't work against viruses.
Adenoviral infections usually don't require
hospitalization.
Prevention
There's no way to completely prevent adenoviral
infections.
To reduce the risk of transmission
hand-washing,
keep shared surfaces such as countertops and
toys clean,
remove human with infections from group
settings until symptoms subside.
Chlorination of swimming pools, drinking water,
wastewater
High hygiene standards in opthamology practice
 Measures to prevent nosocomial transmission
Adenovirus vaccine
 Oral
live attenuated vaccine
 Strains 4, 7
 Used in military recruits
Statistics
Every day in the world infect with HIV 14.000 people,
about 6.000 – young men and women 15 - 24 years old.
Image from http://www.hivaidssearch.com/hiv-aids-links.asp?id=811
Adult Prevalence of AIDS
Image from http://www.hivaidssearch.com/hiv-aids-links.asp?id=811
Human Immunodeficiency Virus
HIV, the etiologjcal agent of AIDS,
belongs to the lentivirus subgroup of the
family Retroviridae.
Structure. HIV is a spherical enveloped
virus, about 90-120 nm in size. The
nucleocapsid has an outer icosaedral shell
and an inner coneshaped core, enclosing
the ribonucleoproteins. The genome is
diploid, composed of two identical single
stranded, positive sense RNA copies.
KEY VIRAL ENZYMES
 Reverse
transcriptase
 Integrase
 Protease
Retrovirus
virion assembly
and release by
budding
some viral proteins
inserted in cell
membrane
host cell chromosome
virus and
cell proteins
in envelope
new viral
genomes and
proteins
provirus
transcription of the
provirus
RNA  DNA
integration into host cell
chromosome
Types of HIV Virus
HIV 1



Most common in sub-Saharan Africa and
throughout the world
Groups M, N, and O
Pandemic dominated by Group M

HIV 2

Group M comprised of subtypes A - J
Most often found in West Central Africa,
parts of Europe and India
Pathogenesis.
The receptor for the virus is the CD4
antigen and therefore the virus may
infect any cell bearing the CD4
antigen on the surface. This is
primarily the T4 (helper/inducer)
lymphocyte.
Some other immune cells also
possess the CD4 antigen on the
surface and so are susceptible to
infection.
Pathogenesis.
Thus about 3 – 10 per cent of B lymphocytes and
10-20 per cent of monocytes and macrophages,
including specialised macrophages such as
alveolar macrophages in the lungs and
Langerhans cells in the dermis are susceptible.
Glial cells and microglia in the central nervous
system are also found infected. Folicular dendritic
cells from tonsils can be infected by HIV without
the involvemnent of CD4.
Specific binding of the virus to CD4 is by
the envelope glycoprotein gp120.
In an infected individual,
HIV can be isolated from
the blood,
lymphocytes,
cell free plasma,
semen,
cervical secretions,
saliva,
tears,
urine
and breast milk.
The primary pathogenic mechanism in
HIV infection is the damage caused to the
T4 lymphocyte. The T4 cells decrease in
numbers and the T4:T8 (helper: killer)
cell ratio is reversed. Viral infection can
suppress the function
of infected cells
without
causing
structural
damage.
Infected T4 cells do not appear to release
normal amounts of interieukin-2, gammainterferon and other lymphokines. This
has a marked dampening effect on cell
mediated immune response.
AIDS
is
primarily
a
sexually
transmitted infection. It was transmitted
predominantly among male homosexuals.
The danger of infection is more for the
passive partner because mucosal tears
are very frequent during anal intercourse
and virus laden lymphocytes in the
semen can directly enter through these.
In homosexual men, the relative risk of
infection in the various sexual practices
has been estimated in the descending
order as ano-receptive, oro-receptive,
ano-insertive and oro-instertive.
PREVENTION OF HIV INFECTION
The second mode of transmission is
through blood and blood products. Before
the danger of HIV transmission was
recognised, many persons had received
blood and blood products containing the
infectious virus. Screening of blood donors
is now mandatory. Even screening may not
completely eliminate the danger as the early
infectious case may be missed but the risk is
reduced considerably.
Contaminated needles can transmit the
infection. This is particularly relevant in
drug addicts who share syringes and
needles.
The use of unsterile syringes and
needles by qualified and unqualified
health workers makes iatrogenic infection
likely. Even in large hospitals, sterilisation
and asepsis are often unsatisfactory. The
use of disposable syringes, needles and
other equipment should be obligatory.
This restriction also applies to the
donation of semen, cornea, bone marrow,
kidney and other organs as infection can be
transmitted through any of these.
Transmission of infection from
mother to baby can take place
before, during or after birth. As
infection occurs in about half such
babies. HIV may be present in
breast milk and may rarely be
transmitted
through
breast
feeding.
How HIV can NOT be transmitted









Through air or by coughing and sneezing
Through food or water
Through sweat and tears
By sharing cups, plates, and utensils with an infected
person
By touching, hugging and kissing an infected person
By sharing clothes or shaking hands with an infected
person
By sharing toilets and bathrooms with an infected person
By living with an infected person
By mosquitoes, fleas, or other insects
101
WHO guidelines for clinical
diagnosis of AIDS in adults
2 major signs & 1 minor sign
(in absence of other explanation)
Major signs:
1. Weight loss > 10% bodyweight
2. Diarrhea > 1 month
3. Fever > 1 month
103
WHO guidelines for clinical
diagnosis of AIDS in an adult
Minor signs:
1. Widespread enlarged lymph glands
2. Persistent cough for more than 1 month
3. Thrush (candida) of mouth & throat
4. Widespread itchy skin rash
5. Recurring shingles (herpes zoster)
6. Chronic, severe, spreading cold sores (HSV1)
7. Loss of memory
8. Loss of intellectual capacity
9. Peripheral nerve damage
104
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© Teaching-ai
Opportunistic Infections

HIV slowly destroys CD4
cells over years of
infection

As the CD4 count drops,
infections take
‘opportunity’ of this
weakened immune
system, resulting in
opportunistic infections
Pneumocystis carinii
Dermatomycosis
Herpes zoster
Dermatitis
Herpes
ACQUIRED DEFICIENCY
SYNDROME (AIDS)
This is the end stage disease representing the
irreversible breakdown of immune defense
mechanisms, leaving the patient a prey to
progressive
opportunistic
infections
and
malignancies. The clinical severity of AIDS varies
with the type of infection or malignancy present.
In early AIDS, many patients are ill only during
episodes of infection which may respond to
treatment. Between
episodes they may be
relatively well and able to resume normal life.
Kaposi's sarcoma
Kaposi's sarcoma
Herpetic infection
Еczema
Warts
Sarcoma
Laboratory diagnosis
Laboratory procedures for the diagnosis of HIV infection
include tests for immunodificiency as well as specific tests
for HIV.
A. Immunological tests. The following parameters help to
establish the immunodeficiency in HIV infection:
l . Total leucocyte and lymphocyte count to demonstrate
leucopenia and a lymphocyte count usually below
2,000 /c.mm.
2. T cell subset assays. Absolute T4 cell count will be
usually less than 200/c.mm. T4: T8 cell ratio is reversed.
3. Platelet count will show thrombocytopenia.
4. Raised IgG and IgA levels.
5. Lymph node biopsy showing profound abnormalities.
CD4 counts

Number of CD4 cells in blood provides a
measure of immune system damage

CD4 count reflects phase of disease

CD4 count:
500 – 1200:
200 – 500:
< 200:
Normal
Beginning of HIV illness
AIDS
122
B. Specific tests for HIV infection. These
inc1ude demonstration of HIV antigens and
antibodies and isolation of the virus.
I. Antigen detection. The time course of
appearance of detectable antigens and antibodies
after VIIV infection is generally as follows:
Following a single massive infection, as by blood
transfusion, the virus antigens (p24) may be
detectable in blood after about two weeks. IgM
antibodies appear in about 4-6 weeks, to be
followed by IgG antibodies.
If the infecting dose is small, as following a
needlestick injury, the process may be considerably
delayed. The appearance of p24 antigenemia and
viremia followed by the early antibody response
coincide with the acute or seroconversion illness.
Afterwards, p24 antigen disappears from circulation
and remains absent during the long asymptomatic
phase, to reappear only when severe clinical disease
sets in. Tests for antigen detection are available only
in specialized laboratories and therefore not used
routinely.
2. Virus isolation. Once infected with HIV, a person
remains infected for life. The virus is present in
circulation and body fluids,
mostly within the
lymphocytes but some are also cell free. Virus titres are
high early in infection, about a week before antibodies
start appearing. Antibodies do not neutralize the virus and
the two can coexist in the body. During the phase of
asymptomatic infection, the virus titre is low and may not
be detectable but when clinical AIDS sets in, the titre
rises once again. An infected person may therefore be
infectious throughout but the infectivity is highest in the
early phase of infection (when the antibody tests are
negative and the case may not be detected in screening
tests) and again when the person becomes clinically ill,
3. Antibody detection. Demonstration of antibodies
is the simplest and most widely employed technique
for the diagnosis of HIV infection. However, it needs
to be emphasized that it may take several weeks to
months for antibodies to appear after infection, and
during the later part of this period, the individual may
be infectious. This seronegative infective stage is
known as the window period. For this reason,
antibody screening is not totally dependable for
spotting infectious persons, for example, from among
blood donors.
Once antibodies appear they increase in titre
and broaden in spectrum for the next
several months. IgM antibodies disappear in
8-10 weeks while IgG antibodies remain
throughout.
When
immunodeficiency
becomes severe following clinical AIDS,
some components of anti HIV antibody
(e.g., anti-p24) may disappear.
Serological tests for anti HIV antibodies are
of two types screening and confirmatory
tests.
Add 1 drop
specimen to well
OraQuick test
HIV Screening Tests
Confirmatory Testing
For
Western blot:
 Venipuncture
for whole blood
 Oral fluid specimen
Follow-up
testing of persons
with negative or indeterminate
Western blot results after 4
weeks
DIAGNOSIS OF HIV INFECTION
EIA
Negative
WESTERN
BLOT
Not indicated
Positive
Negative
Positive
Indeterminate
Positive
Positive
REMARKS
Reassure patient
Re-test in 3
months
Re-test in 3
months or
perform PCR
Counsel and treat
patient
HIV Life Cycle
reverse
transcriptase
inhibitors
like:
Stavudine
Tenofovir
protease
inhibitors
like:
Saquinavir
Darunavir
PREVENTION OF INFECTION