Objectives: HIV-1 generates swarms of similar, but genetically distinct, variants termed quasispecies and many of these variants can be defective. A relevant question is whether such defective species can contribute to viral pathogenesis. Indeed, we previously reported that a presumed recombination of defective proviral DNA with other complementary defective proviral DNA or with wild-type viral DNA in the aftermath of superinfection could lead to the rescue of defective provirus and the production of replication-competent virus. We then wished to determine whether such rescue could be affected by viruses of different subtypes or even by other members of the retrovirus family.
Methods: Here, we have used drug resistance mutations within the HIV genome as markers of potential recombination.
Results: We show that a defective proviral DNA within cells can be rescued by the superinfection of MT2 cells by various subtypes of HIV-1, and by HIV-2 and simian immunodeficiency virus, but not by human T cell leukaemia virus type 1 or by human herpes virus-6. The drug-resistance phenotype of the rescued HIV was confirmed in a second round of infection.
Conclusions: Defective proviral HIV-1 can be rescued by the infection by different variants of HIV-1 and by several other retroviruses as well.
Keywords: HIV recombination; drug resistance; viral latency; viral pathogenesis.