Abstract
Human immunodeficiency virus type 1 (HIV-1) replication is a highly regulated process requiring the recruitment of viral and cellular components to the plasma membrane for assembly into infectious particles. This review highlights the recent process of understanding the selection of the genomic RNA (gRNA) by the viral Pr55Gag precursor polyprotein, and the processes leading to its incorporation into viral particles.
Highlights
Human immunodeficiency virus type 1 (HIV-1) replication is a highly regulated process requiring the recruitment of viral and cellular components to the plasma membrane for assembly into infectious particles
Experiments using inhibitors to block host cell transcription or translation show that simple retroviruses, such as murine leukaemia virus (MLV), segregate unspliced genomic RNA (gRNA) into two functionally distinct populations: one associated with ribosomes for translation and one for packaging into viral particles [43,44,45]
Nuclear magnetic resonance (NMR) structural data showed that the Unique-50 region (U5)–AUG interaction exists in equilibrium with an alternative interaction between the U5 region and the GC-rich loop of stem‐loop 1 (SL1) [16] (Figure 3C)
Summary
Human immunodeficiency virus type 1 (HIV-1) replication is a highly regulated process requiring the recruitment of viral and cellular components to the plasma membrane for assembly into infectious particles. Gag plasma membrane targeting [27,36,37] In this case, efficient normally do not support viral replication due, in part, to inefficient Gag plasma membrane targeting budding could induced upon modifying gRNA export pathway [38,39], or. Efficient normally do not support viral replication due, in part, to inefficient Gag plasma membrane targeting budding could induced upon modifying gRNA export pathway [38,39], or In be this case, efficient budding the could be induced upon modifying thethrough gRNA mutation export of pathway the MA domain to enhance membrane binding [40]. This suggests that RNA export elements can impact later stages of the virus life-cycle through their distinct trafficking behaviours in the cytoplasm
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