scholarly journals Large Evolutionary Rate Heterogeneity among and within HIV-1 Subtypes and CRFs

Viruses ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1689
Author(s):  
Arshan Nasir ◽  
Mira Dimitrijevic ◽  
Ethan Romero-Severson ◽  
Thomas Leitner

HIV-1 is a fast-evolving, genetically diverse virus presently classified into several groups and subtypes. The virus evolves rapidly because of an error-prone polymerase, high rates of recombination, and selection in response to the host immune system and clinical management of the infection. The rate of evolution is also influenced by the rate of virus spread in a population and nature of the outbreak, among other factors. HIV-1 evolution is thus driven by a range of complex genetic, social, and epidemiological factors that complicates disease management and prevention. Here, we quantify the evolutionary (substitution) rate heterogeneity among major HIV-1 subtypes and recombinants by analyzing the largest collection of HIV-1 genetic data spanning the widest possible geographical (100 countries) and temporal (1981–2019) spread. We show that HIV-1 substitution rates vary substantially, sometimes by several folds, both across the virus genome and between major subtypes and recombinants, but also within a subtype. Across subtypes, rates ranged 3.5-fold from 1.34 × 10−3 to 4.72 × 10−3 in env and 2.3-fold from 0.95 × 10−3 to 2.18 × 10−3 substitutions site−1 year−1 in pol. Within the subtype, 3-fold rate variation was observed in env in different human populations. It is possible that HIV-1 lineages in different parts of the world are operating under different selection pressures leading to substantial rate heterogeneity within and between subtypes. We further highlight how such rate heterogeneity can complicate HIV-1 phylodynamic studies, specifically, inferences on epidemiological linkage of transmission clusters based on genetic distance or phylogenetic data, and can mislead estimates about the timing of HIV-1 lineages.

2016 ◽  
Author(s):  
K. Jun Tong ◽  
Sebastián Duchêne ◽  
Nathan Lo ◽  
Simon Y. W. Ho

AbstractGenomes evolve through a medley of mutation, drift, and selection, all of which act heterogeneously across genes and lineages. The pacemaker models of genomic evolution describe the resulting patterns of evolutionary rate variation: genes that are governed by the same pacemaker exhibit the same pattern of rate heterogeneity across lineages. However, the relative importance of drift and selection in determining the structure of these pacemakers is unknown. Here, we propose a novel phylogenetic approach to explain the formation of pacemakers. We apply this method to a genomic dataset from holometabolous insects, an ancient and diverse group of organisms. We show that when drift is the dominant evolutionary process, each pacemaker tends to govern a large number of fast-evolving genes. In contrast, strong negative selection leads to many distinct pacemakers, each of which governs a few slow-evolving genes. Our results provide new insights into the interplay between drift and selection in driving genomic evolution.


2021 ◽  
Vol 9 (1) ◽  
pp. 147
Author(s):  
Ana Santos-Pereira ◽  
Carlos Magalhães ◽  
Pedro M. M. Araújo ◽  
Nuno S. Osório

The already enormous burden caused by Mycobacterium tuberculosis and Human Immunodeficiency Virus type 1 (HIV-1) alone is aggravated by co-infection. Despite obvious differences in the rate of evolution comparing these two human pathogens, genetic diversity plays an important role in the success of both. The extreme evolutionary dynamics of HIV-1 is in the basis of a robust capacity to evade immune responses, to generate drug-resistance and to diversify the population-level reservoir of M group viral subtypes. Compared to HIV-1 and other retroviruses, M. tuberculosis generates minute levels of genetic diversity within the host. However, emerging whole-genome sequencing data show that the M. tuberculosis complex contains at least nine human-adapted phylogenetic lineages. This level of genetic diversity results in differences in M. tuberculosis interactions with the host immune system, virulence and drug resistance propensity. In co-infected individuals, HIV-1 and M. tuberculosis are likely to co-colonize host cells. However, the evolutionary impact of the interaction between the host, the slowly evolving M. tuberculosis bacteria and the HIV-1 viral “mutant cloud” is poorly understood. These evolutionary dynamics, at the cellular niche of monocytes/macrophages, are also discussed and proposed as a relevant future research topic in the context of single-cell sequencing.


2013 ◽  
Vol 19 ◽  
pp. 369-377 ◽  
Author(s):  
Mattias Mild ◽  
Rebecca R. Gray ◽  
Anders Kvist ◽  
Philippe Lemey ◽  
Maureen M. Goodenow ◽  
...  

Science ◽  
1989 ◽  
Vol 246 (4931) ◽  
pp. 808-810 ◽  
Author(s):  
P. Sharp ◽  
D. Shields ◽  
K. Wolfe ◽  
W. Li

Virus Genes ◽  
2018 ◽  
Vol 54 (3) ◽  
pp. 457-460 ◽  
Author(s):  
Naoya Shinohara ◽  
Chieko Matsumoto ◽  
Keiji Matsubayashi ◽  
Tadashi Nagai ◽  
Masahiro Satake

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1112 ◽  
Author(s):  
Samy Sid Ahmed ◽  
Nils Bundgaard ◽  
Frederik Graw ◽  
Oliver Fackler

HIV-1 can use cell-free and cell-associated transmission modes to infect new target cells, but how the virus spreads in the infected host remains to be determined. We recently established 3D collagen cultures to study HIV-1 spread in tissue-like environments and applied iterative cycles of experimentation and computation to develop a first in silico model to describe the dynamics of HIV-1 spread in complex tissue. These analyses (i) revealed that 3D collagen environments restrict cell-free HIV-1 infection but promote cell-associated virus transmission and (ii) defined that cell densities in tissue dictate the efficacy of these transmission modes for virus spread. In this review, we discuss, in the context of the current literature, the implications of this study for our understanding of HIV-1 spread in vivo, which aspects of in vivo physiology this integrated experimental–computational analysis takes into account, and how it can be further improved experimentally and in silico.


Viruses ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 774 ◽  
Author(s):  
Pedro A. Araújo ◽  
Maria O. Freitas ◽  
Jannifer Oliveira Chiang ◽  
Franko Arruda Silva ◽  
Liliane Leal Chagas ◽  
...  

Because of its ecological characteristics, the Caxiuanã National Forest (FLONA) is a potential area of arbovirus circulation. The present study aimed to investigate the occurrence of arbovirus transmission cycles at FLONA de Caxiuanã. Five field trips were performed to capture mosquitoes and sylvatic vertebrates. For these vertebrates, we attempted viral isolation by cell monolayer inoculation from blood, and hemagglutination inhibition and further seroneutralization assays from sera. For mosquitoes, we performed tests of viral genome detection. A total of 338 vertebrates were captured, and the greatest representative was birds (251/74.26%). A total of 16,725 mosquitoes were captured, distributed among 56 species. There were no viruses isolated by newborn mouse inoculation. Among birds, antibodies against Ilheus virus were the most prevalent. Catu virus, Caraparu virus, and Mucambo virus were the most prevalent among mammals and reptiles. Fragments of Mucambo virus, Ilheus virus, Bussuquara virus, and Rocio virus genome were detected in a pool of mosquito samples. These results of the study suggest the occurrence of arbovirus transmission cycles in the FLONA of Caxiuanã. The proximity of human populations with elements, involved in transmission cycles, makes surveillance necessary in this population to avoid dispersion of arboviruses to naïve locations.


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