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Diagnosis and treatment of mutated and evolved variants of HIV
Apr 26, 2004

Can HIV mutate into a strain, subtype etc. that is so different from previous subtypes, that it could elude diagnostic tests in the US...if all HIV antibodies are the same regardlessof genetic composition on the hIV virus that infected someone, why is the HIV -1 test not very reliable in detecting antibodies to HIV-2?

Similarly, could there be mutations of HIV-1 that elude even a bDNA test or even an HIV-1 ELISA test? Is it true that the FDA does not require ELISA tests to be proven effective for detecting antibodies to every subtype, but just the major ones? Do you think thereofre that there is a possibility that there are gaps in testing...that diagnostic tests do not definitely keep pace with the constant genetic mutations and evolutions of HIV? It seems very related too to the issue of drug resistant strains...that more remote genetic variants if HIV may not be as detectable or responsive to existing hAART drugs?

Is it possible that a form of HIV or other retrovirus is out there and,just as HIV-1 took awhile to discover, then HIV-2 and then HIV-1 Groups N and O, that such a retrovirus might lie beneath the radar for now, yet to be isolated.

I would very much appreciate your candid thoughts and expertise on the above.

Many thanks.

Response from Dr. Sherer

HIV is mutating into new strains every day. Remarkably, rather than forming new sub-types, the most common new forms are called CRFs, for circulating recombinant forms, which are mixtures of the currently known subtypes, i.e. A/E ( mix of subtypes A and E), A/G, B/E, etc. Some have components of three or more subtypes.

Fortunately, these mixtures are detectable by the current generation of ELISA antibody tests.

HIV-2 antibodies are not detected by HIV-1 assays because of the different structural element in the virus that leads to antibody formation. There are distinct differences between HIV-1 and HIV-2.

To date, the regions of HIV-1 that form the key elements of ELISA HIV tests are conserved throughout the various sub-types. While what you propose is possible, it has not been observed to date.

And finally, I would urge you not to confuse the issue of the detection of resistant mutations with diagnostic tests for HIV, as they are quite different. We are learning that as we expand the extent of the genome analyzed for resistance tests, possible new sites of mutations which impact replication are identified.

In one case - the 69-S insertion - resistance has been associated with the addition or insertion of new amino acids, rather than a mutation from one to another. Polymorphisms that were once dismissed as playing no role remain an object of intense interest due to the possibility that they may impact resistance in as yet unknown ways.

It is also possible that we are aware of the major pathways for drug resistance. They certainly are complex, varied, and interrelated in innumerable ways.

I agree with one implicit thrust of your question, i.e. that the HIV is highly complex, and has shown repeatedly an ability to frustrate our best attempts to understand and control it. On the other hand, this is an era in which we have proven that the worst of HIV can be overcome with relatively simple steps by people with HIV and their physicians. HIV is due our respect and vigilance, but I advise you not to give it more power than it is due.

still on holiday
trizivir and viread failing?

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