Association of APOBEC3G genotypes and CD4 decline in Thai and Cambodian HIV-infected children with moderate immune deficiency

Bunupuradah, Torsak; Imahashi, Mayumi; Iampornsin, Thatri; Matsuoka, Katsunari; Iwatani, Yoshinori; Puthanakit, Thanyawee; Ananworanich, Jintanat; Sophonphan, Jiratchaya; Mahanontharit, Apicha; Naoe, Tomoki; Saphonn, Vonthanak; Phanuphak, Praphan; Sugiura, Wataru

doi:10.1186/1742-6405-9-34

Cited by 14 publications

(14 citation statements)

References 13 publications

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“…242 Moreover, recent studies found no correlation between the expression levels of A3G and A3F and disease progression in HIV-1 infected children. 243; 244; 245 …”

Section: A3 Restriction In Hiv-1 Infected Patientsmentioning

confidence: 99%

Multiple APOBEC3 Restriction Factors for HIV-1 and One Vif to Rule Them All

Desimmie

Delviks-Frankenberrry

Burdick

et al. 2014

Journal of Molecular Biology

187

214

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Several members of the APOBEC3 family of cellular restriction factors provide intrinsic immunity to the host against viral infection. Specifically, APOBEC3DE, APOBEC3F, APOBEC3G, and APOBEC3H haplotypes II, V, and VII provide protection against HIV-1Δvif through hypermutation of the viral genome, inhibition of reverse transcription, and inhibition of viral DNA integration into the host genome. HIV-1 counteracts APOBEC3 proteins by encoding the viral protein Vif, which contains distinct domains that specifically interact with these APOBEC3 proteins to ensure their proteasomal degradation, allowing virus replication to proceed. Here, we review our current understanding of APOBEC3 structure, editing and non-editing mechanisms of APOBEC3-mediated restriction, Vif-APOBEC3 interactions that trigger APOBEC3 degradation, and the contribution of APOBEC3 proteins to restriction and control of HIV-1 replication in infected patients.

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“…242 Moreover, recent studies found no correlation between the expression levels of A3G and A3F and disease progression in HIV-1 infected children. 243; 244; 245 …”

Section: A3 Restriction In Hiv-1 Infected Patientsmentioning

confidence: 99%

Multiple APOBEC3 Restriction Factors for HIV-1 and One Vif to Rule Them All

Desimmie

Delviks-Frankenberrry

Burdick

et al. 2014

Journal of Molecular Biology

187

214

View full text Add to dashboard Cite

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“…A3G H186R identified in this study was shown in various cohort studies to correlate with disease progression ( An et al, 2004 ; Reddy et al, 2010 ; Singh et al, 2013 ). The variant H186R of A3G is also associated with low CD4 counts ( Bunupuradah et al, 2012 ) and a polymorphism within an A3G intron (C40693T) was shown to correlate with increased risk of infection ( Valcke et al, 2006 ).…”

Section: In Vivo Interactions Of Apobec3s and Hiv-1mentioning

confidence: 99%

AID and APOBECs span the gap between innate and adaptive immunity

2014

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The activation-induced deaminase (AID)/APOBEC cytidine deaminases participate in a diversity of biological processes from the regulation of protein expression to embryonic development and host defenses. In its classical role, AID mutates germline-encoded sequences of B cell receptors, a key aspect of adaptive immunity, and APOBEC1, mutates apoprotein B pre-mRNA, yielding two isoforms important for cellular function and plasma lipid metabolism. Investigations over the last ten years have uncovered a role of the APOBEC superfamily in intrinsic immunity against viruses and innate immunity against viral infection by deamination and mutation of viral genomes. Further, discovery in the area of human immunodeficiency virus (HIV) infection revealed that the HIV viral infectivity factor protein interacts with APOBEC3G, targeting it for proteosomal degradation, overriding its antiviral function. More recently, our and others' work have uncovered that the AID and APOBEC cytidine deaminase family members have an even more direct link between activity against viral infection and induction and shaping of adaptive immunity than previously thought, including that of antigen processing for cytotoxic T lymphocyte activity and natural killer cell activation. Newly ascribed functions of these cytodine deaminases will be discussed, including their newly identified roles in adaptive immunity, epigenetic regulation, and cell differentiation. Herein this review we discuss AID and APOBEC cytodine deaminases as a link between innate and adaptive immunity uncovered by recent studies.

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“…In contrast, no correlation has been observed between disease progression and A3G/A3F expression or hypermutation levels [ 25 ]. However, a genetic variant of the A3G genotype, H186 in GG, was significantly associated with more rapid declines in CD4+ T cell counts over time in ART-naïve HIV-infected Thai and Cambodian children with moderate immunodeficiency [ 26 ]. Recently, the A3G-H186R and F119F variants were also shown to be associated with altered HIV-1-related disease progression and central nervous system impairment in a cohort of 1,049 HIV-infected children [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Innate Antiviral Restricting Factor Expression in the Cord Blood and Decidual Tissue of HIV-Infected Mothers

et al. 2013

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Programs for the prevention of mother-to-child transmission of HIV have reduced the transmission rate of perinatal HIV infection and have thereby increased the number of HIV-exposed uninfected (HEU) infants. Natural immunity to HIV-1 infection in both mothers and newborns needs to be further explored. In this study, we compared the expression of antiviral restricting factors in HIV-infected pregnant mothers treated with antiretroviral therapy (ART) in pregnancy (n=23) and in cord blood (CB) (n=16), placental tissues (n=10-13) and colostrum (n=5-6) samples and compared them to expression in samples from uninfected (UN) pregnant mothers (n=21). Mononuclear cells (MNCs) were prepared from maternal and CB samples following deliveries by cesarean section. Maternal (decidua) and fetal (chorionic villus) placental tissues were obtained, and colostrum was collected 24 h after delivery. The mRNA and protein expression levels of antiviral factors were then evaluated. We observed a significant increase in the mRNA expression levels of antiviral factors in MNCs from HIV-infected mothers and CB, including the apolipoprotein B mRNA-editing enzyme 3G (A3G), A3F, tripartite motif family-5α (TRIM-5α), TRIM-22, myxovirus resistance protein A (MxA), stimulator of interferon (IFN) genes (STING) and IFN-β, compared with the levels detected in uninfected (UN) mother-CB pairs. Moreover, A3G transcript and protein levels and α-defensin transcript levels were decreased in the decidua of HIV-infected mothers. Decreased TRIM-5α protein levels in the villi and increased STING mRNA expression in both placental tissues were also observed in HIV-infected mothers compared with uninfected (UN) mothers. Additionally, colostrum cells from infected mothers showed increased tetherin and IFN-β mRNA levels and CXCL9 protein levels. The data presented here indicate that antiviral restricting factor expression can be induced in utero in HIV-infected mothers. Future studies are warranted to determine whether this upregulation of antiviral factors during the perinatal period has a protective effect against HIV-1 infection.

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Association of APOBEC3G genotypes and CD4 decline in Thai and Cambodian HIV-infected children with moderate immune deficiency

Cited by 14 publications

References 13 publications

Multiple APOBEC3 Restriction Factors for HIV-1 and One Vif to Rule Them All

Multiple APOBEC3 Restriction Factors for HIV-1 and One Vif to Rule Them All

AID and APOBECs span the gap between innate and adaptive immunity

Upregulation of Innate Antiviral Restricting Factor Expression in the Cord Blood and Decidual Tissue of HIV-Infected Mothers

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