Abstract
The lentiviral envelope glycoproteins (Env) mediate virus entry by interacting with specific receptors present at the cell surface, thereby determining viral tropism and pathogenesis. Therefore, Env incorporation into the virions formed by assembly of the viral Gag polyprotein at the plasma membrane of the infected cells is a key step in the replication cycle of lentiviruses. Besides being useful models of human immunodeficiency virus (HIV) infections in humans and valuable tools for developing AIDS therapies and vaccines, simian and feline immunodeficiency viruses (SIV and FIV, respectively) are relevant animal retroviruses; the study of which provides important information on how lentiviral replication strategies have evolved. In this review, we discuss the molecular mechanisms underlying the incorporation of the SIV and FIV Env glycoproteins into viral particles.
Highlights
Lentiviruses, members of the Retroviridae family, can be classified into two groups based on their cellular tropism and disease manifestations [1]
feline immunodeficiency virus (FIV) is a lentivirus that induces in domestic cats an AIDS-like disease similar to that caused by human immunodeficiency virus (HIV)-1 in humans [92]
In addition to its role in membrane targeting and association of the Gag polyprotein with the plasma membrane, the simian immunodeficiency virus (SIV) MA domain participates in the process of envelope glycoprotein (Env) incorporation into virions
Summary
Lentiviruses, members of the Retroviridae family, can be classified into two groups based on their cellular tropism and disease manifestations [1]. The pol genes of nonprimate lentiviruses have evolved to contain an additional genetic element coding for dUTPase activity which prevents the incorporation of uracil into the reverse-transcribed viral DNA products [2] In addition to these genes, lentiviral genomes exhibit a series of overlapping small open reading frames coding for regulatory proteins. In this regard, HIV and SIV are unique among lentiviruses because their genomes contain the largest number of auxiliary genes, namely tat, rev, vif, nef, vpu, vpr and vpx, the products of which are involved in the transcription of the viral genome, RNA processing, and in counteracting the antiviral activity of cell host restriction factors [3,4]. We review our current understanding of Env packaging into lentiviral particles focusing on SIV and FIV, since this process has been extensively and comprehensively discussed for HIV-1 in recent articles [17,18,19]
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