RTB: HIV tests come up positive for everything. Here researchers find that ‘specific’ HIV test proteins are…yes, non-specific. Again. And again. And again. But, they note, anyone with an ‘autoimmune disease’ should always be tested for “HIV!”
What about the ‘false’ results? They declare using a Western Blot should sort it out. Never mind that Western Blots contain precisely the same proteins as ELISA tests. Never mind that they have no standards for interpretation from lab to lab, country to country; or that some countries, like the UK, won’t use them because they consider them so awful!
But because the tests are so awful, they ‘suggest’ using PCR. Which work just as well. Ehm…badly. You can read about the wonders of PCR Here – these tests also have no standard, give no reproducible results, and come up positive and negative in the same sample from lab to lab, hour to hour, minute to minute. It’s a real ‘wheel of fortune’ with “HIV Testing.”
M H Esteva, A M Blasini, D Ogly and M A Rodri?guez?Ann Rheum Dis 1992;51;10711073 doi:10.1136/ard.51.9.1071
Abstract: False positive results were obtained for HIV tests in two men with active systemic lupus erythematosus (SLE) who were suspected of being infected with HIV because of fever, weight loss, lymphadenopathy, and inflammatory myopathy. Enzyme linked immuno sorbent assays (ELISAs) for HIV were twice positive when tested three times over a period of six months.Western blot analysis showed reactivity against the gp4l band in patient 1. False positive results for HIV tests can occur in patients with SLE, potentially leading to an erroneous diagnosis of HIV infection.
Interestingly Golding et al’2 showed cross reacting antibodies recognising the HIV gp41 protein and the 13 domain of human major histocompatibility complex class II molecules in serum samples from patients with AIDS. Okudaira et all’ have reported the presence of antibodies to HLADR molecules in serum from patients with SLE. It is possible that serum samples from patient 1 had this pattern of cross reacting antibodies in the absence of HIV infection. Antibodies to the p24 gag protein of HIV1 have also been reported in patients with SLE.’4 Whether these antibodies arise by molecular mimicry to homologous host proteins or reflect viral infection remains to be established.
The diagnosis of HIV infection should always be considered in patients presenting with clinical symptoms suggestive of asystemic autoimmune disease. The use of rigorous confirmatory testing by western blot analysis or immuno fluorescence assay is therefore mandatory. More sensitive assays such as gene amplification by the polymerase chain reaction may be necessary to confirm the presence of HIV infection in patients with unclear serological reactions.