(Human

Immuno-
deficien
cy Virus)
Retno Budiarti, dr. MKes
Microbiology department
Medical Facultly
Hang Tuah University
virology
• Icosahedral (20 sided), enveloped virus of the lentivirus
subfamily of retroviridae.
• Retroviruses transcribe RNA to DNA.
• Two viral strands of RNA found in core surrounded by
protein outer coat
• outer envelope contains a lipid matrix within which specific viral
glycoproteins are imbedded
• These knob-like structures responsible for binding to target cell.

virology
• HIV can infect T4 lymphocytes and other cells bearing
the CD4 marker on their surface.
• The CD4 molecule is the main receptor for HIV, or more
precisely for its gp120
• In addition, either the chemokine receptor CCR5
(macrophage-tropic R5 HIV strains) or CXCR4 (T cell-
tropic X4 strains) is used as a coreceptor.

attachment
• Persons with (homozygotic) missing CCR5 are highly
resistant to HIV infection.
• A number of other coreceptors are also active depending
on the viral strain involved.

attachment
from blood from blood from culture
 • In early phase HIV
infection, initial viruses
are M-tropic. Their
envelope glycoprotein
gp120 is able to bind to
CD4 molecules and
chemokine receptors
called CCR5 found on
macrophages

replication
• In late phase HIV
infection, most of the
viruses are T-tropic,
having gp120 capable
of binding to CD4 and
CXCR4 found on T4-
lymphocytes
• The gp120 protein on virus binds specifically to CD4
receptor on host cell with high affinity.
• Gp41 causes fusion of the virus to the cell membrane.
• After fusion virus particle enters cell.
• Viral genome exposed by uncoating particle.
• Reverse transcriptase produces viral DNA from RNA.
• Becomes a provirus which integrates into host DNA.
• Period of latency occurs.
• After a period of latency lasting up to 10 years viral
replication is triggered and occurs at high rate.
• CD4 cell may be destroyed in the process, body attempts
to replace lost CD4 cells, but over the course of many
years body is unable to keep the count at a safe level.
• Destruction of large numbers of CD4 cause symptoms of
HIV to appear with increased susceptibility to
opportunistic infections, disease and malignancy.
• HIV is then taken in by the cell.
• After uncoating, reverse transcription takes place in the
cytoplasm.
• The interaction of the many different contributing control
genes is responsible for the long latency period and
subsequent viral replication
• Replication of HIV takes the form of a lytic cycle, i.e., it
results in destruction of the host cell
• It must also be noted that the cell destruction mechanism
has not been completely explained.
• Cell fusions are induced by X4 strains (syncytial
formation).
transmission
virus particles are bound by dendritic cells (DC)s as
APC through the C-type lectin receptor (CLR) DC-
SIGN
Virus or virus-infected cells then reach the draining
lymph nodes, where activated CD4+CCR5+ T
• The profound immunosuppression seen in AIDS is due to the
depletion of T4 helper lymphocytes.
• In the immediate period following exposure, HIV is present at
a high level in the blood (as detected by HIV Antigen and HIV-
RNA assays).
• During the incubation period, there is a massive turnover of
CD4 cells, whereby CD4 cells killed by HIV are replaced
efficiently.
• Eventually, the immune system succumbs and AIDS develop
when killed CD4 cells can no longer be replaced (witnessed by
high HIV-RNA, HIV-antigen, and low CD4 counts).

pathogenesis
• HIV continues to reproduce, CD4 count
gradually declines from its normal value of 500-
1200.
• Once CD4 count drops below 500, HIV infected
person at risk for opportunistic infections.
• The following diseases are predictive of the
progression to AIDS:
• persistent herpes-zoster infection (shingles)
• oral candidiasis (thrush)
• oral hairy leukoplakia
• Kaposi’s sarcoma (KS)

Clinical Latency Period

Kaposi’s sarcoma (shown) is a
rare cancer of the blood vessels
that is associated with HIV. It
manifests as bluish-red oval-
shaped patches that may
eventually become thickened.
Lesions may appear singly or in
clusters.
Thank you……