Open AccessFew amino acid signatures distinguish HIV-1 subtype B pandemic and non-pandemic strains
Author(s) -
Ighor Arantes,
Marcelo Ribeiro-Alves,
Suwellen Sardinha Dias de Azevedo,
Edson Delatorre,
Gonzalo Bello
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0238995
Subject(s) - pandemic , virology , biology , clade , human immunodeficiency virus (hiv) , virus , genetics , sequence analysis , phylogenetics , covid-19 , gene , medicine , disease , pathology , infectious disease (medical specialty)
The Human Immunodeficiency Virus Type I (HIV-1) subtype B comprises approximately 10% of all HIV infections in the world. The HIV-1 subtype B epidemic comprehends a pandemic variant (named B PANDEMIC ) disseminated worldwide and non-pandemic variants (named B CAR ) that are mostly restricted to the Caribbean. The goal of this work was the identification of amino acid signatures (AAs) characteristic to the B CAR and B PANDEMIC variants. To this end, we analyzed HIV-1 subtype B full-length (n = 486) and partial (n = 814) genomic sequences from the Americas classified within the B CAR and B PANDEMIC clades and reconstructed the sequences of their most recent common ancestors (MRCA). Analysis of contemporary HIV-1 sequences revealed 13 AAs between B CAR and B PANDEMIC variants (four on Gag, three on Pol, three on Rev, and one in Vif, Vpu, and Tat) of which only two (one on Gag and one on Pol) were traced to the MRCA. All AAs correspond to polymorphic sites located outside essential functional proteins domains, except the AAs in Tat. The absence of stringent AAs inherited from their ancestors between modern B CAR and B PANDEMIC variants support that ecological factors, rather than viral determinants, were the main driving force behind the successful spread of the B PANDEMIC strain.