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. Author manuscript; available in PMC: 2012 Aug 27.
Published in final edited form as: Curr HIV/AIDS Rep. 2009 Feb;6(1):5–12. doi: 10.1007/s11904-009-0002-3

Table 1.

Relations between coinfecting viruses and HIV-1

Virus Mechanisms Potential effects on HIV-1*
HBV Several anti-HBV drugs are also HIV-1 RT inhibitors HBV treatment also decreases HIV replication; emergence of HIV-1 RT-resistant mutants
HCV Systemic immune activation Facilitation of HIV-1 replication
GBV-C CCR5 and CXCR4 downregulation; induction of RANTES and SDF-1 Suppression of HIV-1 replication
HTLV-1 LTR transactivation; induction of CC chemokines Facilitation of HIV-1 replication; suppression of HIV-1 R5 replication
HTLV-2 Induction of CC chemokines; decreased systemic immune activation Suppression of HIV-1 replication
HIV-2 Cross-reactive immune response; induction of CC chemokines Decreased HIV-1 acquisition; suppression of HIV-1 R5 replication
JCV Suppression of Tat functions Suppression of HIV-1 replication in vitro
Measles virus Induction of RANTES; blockage of CD4 T-cell cycle Suppression of HIV-1 replication
HSV-2 Genital ulceration; increased LTR transactivation Increased HIV-1 transmission; facilitation of HIV-1 replication
CMV Increased HIV-1 load in semen; induction of chemokines, virokines, and viroceptors Increased HIV-1 transmission; variable results were reported for the net effect
HHV-6 Induction of RANTES, virokines, LTR transactivation, CD3 and CD46 downregulation Decreased replication of HIV-1 R5 ex vivo; net effect on HIV-1 replication in vivo to be studied
HHV-7 Downregulation of CD4 Decreased replication of HIV-1 R5 ex vivo; net effect on HIV-1 replication in vivo to be studied
HHV-8 Chemokines and virokines Net effect of HIV-1 replication in vivo to be studied
*

In vivo, some of the potential effects of coinfecting microbes on HIV-1, especially those that were identifi ed in in vitro system only, may be masked (eg, due to several opposite signals triggered by the same or different microbes, or by other host factors that determine HIV disease). CMV—cytomegalovirus; GBV-C—GB virus C; HBV—hepatitis B virus; HCV—hepatitis C virus; HHV—human herpesvirus; HSV—herpes simplex virus; HTLV—human T-cell leukemia virus; JCV—JC virus; LTR—long terminal repeat; RANTES—regulated upon activation, normal T-cell expressed and secreted; RT—reverse transcriptase; SDF—stromal cell-derived factor.