A novel antiviral strategy for HIV infection.
The replication of human immunodeficiency virus (HIV) may be modulated in part by host factors such as DNA methylation. Hypermethylation of the HIV provirus may suppress viral replication and play a role in the establishment of latency. HIV seropositive individuals have decreased levels of metabolites involved in methylation. It is proposed that metabolites such as S-adenosylmethionine (SAM), methylcobalamin and methyltetrahydrofolate be explored as potential therapeutic agents in HIV infected individuals.
May
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D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy* / Q000378:metabolism; D004279:DNA, Viral / Q000378:metabolism; D006678:HIV / Q000472:pathogenicity / Q000502:physiology*; D015658:HIV Infections / Q000188:drug therapy* / Q000378:metabolism; D006679:HIV Seropositivity / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D008745:Methylation; D011533:Proviruses / Q000502:physiology; D012436:S-Adenosylmethionine / Q000378:metabolism; D013763:Tetrahydrofolates / Q000627:therapeutic use; D014779:Virus Replication; D014805:Vitamin B 12 / Q000031:analogs & derivatives / Q000627:therapeutic use
D004279:DNA, Viral; D013763:Tetrahydrofolates; D012436:S-Adenosylmethionine; C019476:mecobalamin; D014805:Vitamin B 12; C005984:5-methyltetrahydrofolate