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Human immunodeficiency virus exploits cells central to adaptive immunity,
converting their molecular machinery into a means of viral replication.
Entry begins when the envelope glycoprotein gp120 binds the CD4 receptor.
A conformational change then exposes the co-receptor binding site.
Macrophage-tropic strains use CCR5, whereas T-cell-tropic strains use CXCR4,
and gp41 drives fusion of the viral and cellular membranes.
Reverse transcriptase copies the RNA genome into DNA,
and integrase inserts it into the host chromosome as a provirus.
People homozygous for the CCR5 delta-32 deletion resist R5 strains,
and maraviroc mimics that deletion pharmacologically.
Years of chronic viraemia follow,
during which billions of virions are produced daily
and CD4 cells are progressively depleted.
Diagnosis depends on knowing what each assay can and cannot see.
The fourth-generation antigen and antibody immunoassay is highly sensitive but not confirmatory,
so a reactive result requires a differentiation assay
or Western blot before notification.
In acute infection,
antibody and even p24 antigen may be absent for the first weeks.
Only HIV RNA reliably detects this window,
and it should be requested whenever a compatible illness follows a recent exposure.
All reactive HIV screening tests require a confirmatory assay,
and acute infection is detected by HIV RNA rather than antibody.
Is the CD4 count below 200?
Then Pneumocystis prophylaxis with co-trimoxazole begins,
and below 100 the same drug covers Toxoplasma.
On treatment,
an undetectable viral load sustained for six months means the virus cannot be transmitted
sexually.
Lucid rule for tuberculosis:
start antiretrovirals within two weeks when the CD4 count is below 50,
but wait four to eight weeks in meningitis.
The CD4 count is a clock,
and each threshold uncovers a different pathogen.
Below 200 cells per microlitre, Pneumocystis pneumonia appears,
prevented and treated with co-trimoxazole.
Below 100, Toxoplasma encephalitis and cryptococcal meningitis emerge.
Below 50, cytomegalovirus retinitis and disseminated Mycobacterium avium complex follow.
Tuberculosis, candidiasis, zoster and Kaposi sarcoma can occur at any count.
A CD4 count below 200 defines AIDS by itself.
Non-Hodgkin lymphoma, Kaposi sarcoma and invasive cervical cancer are AIDS-defining,
whereas Hodgkin lymphoma, although more frequent, is not.
Antiretroviral therapy should start as soon as possible after diagnosis,
regardless of CD4 count.
Current Australian guidance prefers an integrase inhibitor such as bictegravir combined with emtricitabine
and tenofovir alafenamide.
Sustained suppression restores CD4 cells and eliminates sexual transmission.
The PARTNER studies recorded no linked transmissions from partners with an undetectable viral load,
the basis of undetectable equals untransmittable.
Without treatment,
vertical transmission occurs in about 25 to 30 per cent of pregnancies.
With suppressive therapy it falls below one per cent.
Tuberculosis co-infection demands sequencing.
Tuberculosis treatment starts first,
and antiretroviral therapy follows within two weeks
when the CD4 count is below 50.
At higher counts it may be started within eight weeks,
but tuberculous meningitis is the exception.
There,
therapy is deferred for four to eight weeks
because intracranial immune reconstitution raises mortality.
Rifampicin, a potent CYP3A4 inducer, renders boosted protease inhibitors sub-therapeutic.
Rifabutin, or an alternative regimen, is substituted.
All reactive HIV screening tests require a confirmatory assay,
and acute infection is detected by HIV RNA rather than antibody.
Is the CD4 count below 200?
Then Pneumocystis prophylaxis with co-trimoxazole begins,
and below 100 the same drug covers Toxoplasma.
On treatment,
an undetectable viral load sustained for six months means the virus cannot be transmitted
sexually.
Lucid rule for tuberculosis:
start antiretrovirals within two weeks when the CD4 count is below 50,
but wait four to eight weeks in meningitis.