ABSTRACT
Human immunodeciency virus (HIV) is an enveloped lentivirus of the Retroviridae family characterized by two single-stranded RNA genomes enclosed inside of a capsid and viral replication through the enzyme reverse transcriptase [1-3]. On its surface are exterior, transmembrane glycoproteins referred to as gp120 and gp41, respectively (or as env or gp160 collectively), which are responsible for cellular entry [4,5]. HIV consists of two types, HIV-1 and HIV-2. While both have similar modes of transmission, HIV-1 is predominant and more virulent, and HIV-2 is less virulent, causing a milder disease that progresses more slowly [6]. HIV-1 is highly diverse, consisting of three major groups (M: “Major” or “Main”, O: “Outlier”, and N: “Nonmajor and Nonoutlier” or “New”), and a new minor group P rst reported in 2009, various subtypes or clades (A-D, F-H, J, and K; only for group M), several sub-subtypes (A1-A4, F1, and F2), and 48 (Los Alamos HIV Database, https://www.hiv.lanl.gov/content/ sequence/HIV/CRFs/CRFs.html) circulating recombinant forms (CRFs) resulting from recombination of different subtypes or strains [7-9]. HIV presents many challenges due to its ability to rapidly evolve, mutate, and develop drug-resistance. Due to the lack of proofreading activity of HIV reverse transcriptase, a high-turnover rate of replication, and the persistent recombination of different HIV-1 genomes, millions of viral variants are produced within an infected person daily, and genetic variations within any given subtype is believed to be as high as 20% [10,11].
