Env length and N-linked glycosylation following transmission of human immunodeficiency virus Type 1 subtype B viruses

Liu, Yi; Curlin, Marcel E.; Diem, Kurt; Zhao, Hong; Ghosh, Ananta K.; Zhu, Haiying; Woodward, Amanda; Maenza, Janine; Stevens, Claire E.; Stekler, Joanne D.; Collier, Ann C.; Genowati, Indira; Deng, Wenjie; Zioni, Rafael; Corey, Lawrence; Zhu, Tuofu; Mullins, James I.

doi:10.1016/j.virol.2008.01.029

Cited by 73 publications

(85 citation statements)

References 18 publications

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“…We and others have reported that founder viruses generally have fewer glycosylation sites and more compact Envs (9,(31)(32)(33), and our earlier studies also demonstrated that newly transmitted viruses were not escape variants from PL-neutralizing antibodies in the donor (9). Recent studies have suggested that subtype A and C founder viruses bind efficiently to the gut homing receptor α4β7 expressed on a subset of highly susceptible CD4 T lymphocytes and that this property can be reduced with evolution of the virus after transmission (34).…”

Section: Discussionmentioning

confidence: 61%

Role of donor genital tract HIV-1 diversity in the transmission bottleneck

Boeras

Hraber

Hurlston

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

106

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The predominant mode of HIV-1 infection is heterosexual transmission, where a genetic bottleneck is imposed on the virus quasispecies. To probe whether limited genetic diversity in the genital tract (GT) of the transmitting partner drives this bottleneck, viral envelope sequences from the blood and genital fluids of eight transmission pairs from Rwanda and Zambia were analyzed. The chronically infected transmitting partner's virus population was heterogeneous with distinct genital subpopulations, and the virus populations within the GT of two of four women sampled longitudinally exhibited evidence of stability over time intervals on the order of weeks to months. Surprisingly, the transmitted founder variant was not derived from the predominant GT subpopulations. Rather, in each case, the transmitting variant was phylogenetically distinct from the sampled locally replicating population. Although the exact distribution of the virus population present in the GT at the time of transmission cannot be unambiguously defined in these human studies, it is unlikely, based on these data, that the transmission bottleneck is driven in every case by limited viral diversity in the donor GT or that HIV transmission is solely a stochastic event.

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Section: Discussionmentioning

confidence: 61%

Role of donor genital tract HIV-1 diversity in the transmission bottleneck

Boeras

Hraber

Hurlston

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

106

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“…Furthermore, reanalyzing other published transmission pairs with known or assumed direction showed mostly PM/consistent, some PP, and a few MM phylogenies (18,33,43,44). Likewise, in known transmission chains, involving several persons with multiple sampled clones per patient, again most transmissions seemed to be PM/consistent with a few MM topologies among patients that had infected each other, whereas among patients that had not directly infected each other the topology always was MM (19,45).…”

Section: Paraphyletic Signal Predicts Direction Of Transmission But Dmentioning

confidence: 88%

Phylogenetically resolving epidemiologic linkage

Romero-Severson

Bulla

Leitner

2016

Proc. Natl. Acad. Sci. U.S.A.

134

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Although the use of phylogenetic trees in epidemiological investigations has become commonplace, their epidemiological interpretation has not been systematically evaluated. Here, we use an HIV-1 within-host coalescent model to probabilistically evaluate transmission histories of two epidemiologically linked hosts. Previous critique of phylogenetic reconstruction has claimed that direction of transmission is difficult to infer, and that the existence of unsampled intermediary links or common sources can never be excluded. The phylogenetic relationship between the HIV populations of epidemiologically linked hosts can be classified into six types of trees, based on cladistic relationships and whether the reconstruction is consistent with the true transmission history or not. We show that the direction of transmission and whether unsampled intermediary links or common sources existed make very different predictions about expected phylogenetic relationships: (i) Direction of transmission can often be established when paraphyly exists, (ii) intermediary links can be excluded when multiple lineages were transmitted, and (iii) when the sampled individuals' HIV populations both are monophyletic a common source was likely the origin. Inconsistent results, suggesting the wrong transmission direction, were generally rare. In addition, the expected tree topology also depends on the number of transmitted lineages, the sample size, the time of the sample relative to transmission, and how fast the diversity increases after infection. Typically, 20 or more sequences per subject give robust results. We confirm our theoretical evaluations with analyses of real transmission histories and discuss how our findings should aid in interpreting phylogenetic results.HIV-1 | transmission | paraphyly | coalescent | phylogeny

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“…In horizontal transmission, acutely infected subjects were found to have shorter variable loops and fewer PNG sites encoded in env compared to subjects with chronic HIV-1 infection for subtypes A and C, but not subtype B (10,32,34). In vertical transmission, one study of an HIV-1 subtype CRF_AE-infected cohort found no difference in sequence length or PNG sites, while in other studies analyzing multiple subtypes there were fewer PNG sites in transmitted viruses (47,59).…”

Section: Subtype C Human Immunodeficiency Virus Type 1 (Hiv-1c) Contimentioning

confidence: 98%

The Genetic Bottleneck in Vertical Transmission of Subtype C HIV-1 Is Not Driven by Selection of Especially Neutralization-Resistant Virus from the Maternal Viral Population

Russell¹,

Kwiek

Keys

et al. 2011

J Virol

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Subtype C human immunodeficiency virus type 1 (HIV-1C) continues to cause the majority of new cases of mother-to-child transmission (MTCT), and yet there are limited data on HIV-1C transmission. We amplified env from plasma RNA for 19 HIV-1C MTCT pairs, 10 transmitting in utero (IU) and 9 transmitting intrapartum (IP). There was a strong genetic bottleneck between all mother-infant pairs, with a majority of transmission events involving the transmission of a single virus. env genes of viruses transmitted to infants IP, but not IU, encoded Env proteins that were shorter and had fewer putative N-linked glycosylation sites in the V1-V5 region than matched maternal sequences. Viruses pseudotyped with env clones representative of each maternal and infant population were tested for neutralization sensitivity. The 50% inhibitory concentration of autologous serum was similar against both transmitted (infant) and nontransmitted (maternal) viruses in a paired analysis. Mother and infant Env proteins were also similar in sensitivity to soluble CD4, to a panel of monoclonal antibodies, and to heterologous HIV-1C sera. In addition, there was no difference in the breadth or potency of neutralizing antibodies between sera from 50 nontransmitting and 23 IU and 23 IP transmitting HIV-1C-infected women against four Env proteins from heterologous viruses. Thus, while a strong genetic bottleneck was detected during MCTC, with viruses of shorter and fewer glycosylation sites in env present in IP transmission, our data do not support this bottleneck being driven by selective resistance to antibodies.

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Env length and N-linked glycosylation following transmission of human immunodeficiency virus Type 1 subtype B viruses

Cited by 73 publications

References 18 publications

Role of donor genital tract HIV-1 diversity in the transmission bottleneck

Role of donor genital tract HIV-1 diversity in the transmission bottleneck

Phylogenetically resolving epidemiologic linkage

The Genetic Bottleneck in Vertical Transmission of Subtype C HIV-1 Is Not Driven by Selection of Especially Neutralization-Resistant Virus from the Maternal Viral Population

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