An endogenous retrovirus is one whose genetic material has been incorporated into that of the host. This happens when the genome of the virus incorporates itself into the chromosome of the host's sex cell (sperm or egg) – or its progenitor – and thus, upon fertilization becomes part of the normal genome found in every cell in the body of the host. Over time, the endogenous retroviral genome usually accumulates deleterious mutations rendering it incapable of productive infection. One myth used by denialists is that HIV is one of these endogenous retroviruses. However, several lines of evidence from the published scientific literature refute this claim, and prove that it is an exogenous virus, found only in CD4+ T-cells and a few other CD4+ cell types (such as macrophages) and not found in most other host cells.
In the very first publication regarding the identification of HIV, Dr. Luc Montagnier described several experiments showing that HIV was exogenous. The controls used in his co-culture experiments, for example, did not produce a reverse transcriptase signal, only those cells exposed to infected patient lymphocytes. This indicates that the signal did not originate from the genome of the uninfected donor cells. The RT signal (and thus the virus) was able to be passed on to other uninfected lymphocyte cultures and resulted in a similar RT signal pattern. This passing on of the virus is another line of evidence that HIV is unlikely to be endogenous [1].
The southern blot is a method for probing for the presence of a specific DNA sequence within a DNA sample. In southern blot hybridization, a small segment of single-stranded DNA is hybridized to genomic DNA. There is nothing in the human genome that hybridizes at reasonable stringency levels (i.e. the specificity of the test) to probes made from HIV-1 or HIV-2 proviral genomes[2]. One study did find two very short sequences (192bp and ~30bp) with some similarity (<60% and 95% respectively) to parts of the HIV genome. However, these two sequences were detected only under very low stringency (low specificity) and no other sequences with similarity to HIV were found [3].
In experiments using PCR (another method for detecting specific genetic sequences) in infected patients’ lymphocytes, PCR detects HIV in only a fraction of the infected donor’s T-Cells [4]. This alone is enough to demonstrate that HIV cannot be endogenous. An endogenous virus, by virtue of its past integration in host germ cells, would be detectable in all nucleated cells of the host. In other experiments, HIV DNA was found in the lymphocytes of patients but only very rarely in sperm cells [5]. The absence of HIV DNA from certain cell types in patients again refutes the idea that HIV is endogenous.
The genome projects have been a valuable tool in the field of genetics and also refute the idea that HIV is endogenous. At the time this article was being written, only two examples existed in the scientific literature of endogenous lentiviruses in mammals: one in rabbits and one in lemurs [6][7]. All sequenced primate genomes (including several human genomes) show no endogenous lentiviral genomes.
Some common sense combined with a brief look at infections would likewise indicate that HIV is not endogenous. If it were endogenous, sequences would be most similar between family members and most different between distantly related individuals. However, this is not the case. Europeans of non-West African descent have been identified with HIV-2 infection, despite HIV-2 being predominantly found in West Africa [8]. Conversely, many Africans have been infected by HIV-1. If one claims that HIV is endogenous, one therefore also claims that West Africans with HIV-2 infections are more closely related to non-West African Europeans with HIV-2 infection than they are to their HIV-1 infected countrymen. This is simply absurd.
1. Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS). Barré-Sinoussi F, Chermann JC, Rey F, Nugeyre MT, Chamaret S, Gruest J, Dauguet C, Axler-Blin C, Vézinet-Brun F, Rouzioux C, Rozenbaum W, Montagnier L. Science. 1983 May 20;220(4599):868-71. PMID: 6189183
2. Characterization of a continuous T-cell line susceptible to the cytopathic effects of the acquired immunodeficiency syndrome (AIDS)-associated retrovirus. Folks T, Benn S, Rabson A, Theodore T, Hoggan MD, Martin M, Lightfoote M, Sell K. Proc Natl Acad Sci U S A. 1985 Jul;82(13):4539-43. PMID: 2989831
3. Novel human endogenous sequences related to human immunodeficiency virus type 1. Horwitz MS, Boyce-Jacino MT, Faras AJ. J Virol. 1992 Apr;66(4):2170-9. PMID: 1548756
4. Sensitive detection of HIV DNA in T4 lymphocytes of infected individuals by polymerase chain reaction.
Hsia K, Spector SA; International Conference on AIDS. Int Conf AIDS. 1990 Jun 20-23; 6: 160
5. HIV-particles in spermatozoa of patients with AIDS and their transfer into the oocyte. Baccetti B, Benedetto A, Burrini AG, Collodel G, Ceccarini EC, Crisà N, Di Caro A, Estenoz M, Garbuglia AR, Massacesi A, et al. J Cell Biol. 1994 Nov;127(4):903-14. PMID: 7962075
6. Discovery and analysis of the first endogenous lentivirus. Aris Katzourakis, Michael Tristem, Oliver G. Pybus, and Robert J. Gifford Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6261–6265. PMCID: PMC1851024
7. Parallel Germline Infiltration of a Lentivirus in Two Malagasy Lemurs. Gilbert C, Maxfield DG, Goodman SM, Feschotte C, 2009 PLoS Genet 5(3): e1000425. doi:10.1371/journal.pgen.1000425
8. HIV-2 infection in 12 European residents : virus characteristics and disease progression. Van Der Ende M. E.; Schutten M.; Thaoi Duong LY; Gruters R. A.; Osterhaus A. D. M. E. AIDS ISSN 0269-9370 1996, vol. 10, no14, pp. 1649-1655 (23 ref.)
