Abstract
Studies of the human immunodeficiency virus type 1 (HIV-1) continue to enrich eukaryotic biology and immunology. Recent advances have defined factors that function after viral entry and prevent the replication of proviruses in the infected cell. Some of these attack directly viral structures whereas others edit viral genetic material during reverse transcription. Together, they provide strong and immediate intracellular immunity against incoming pathogens. These processes also offer a tantalizing glimpse at basic cellular mechanisms that might restrict the movement of mobile genetic elements and protect the genome.
Highlights
It is highly pathogenic in humans, human immunodeficiency virus type 1 (HIV-1) cannot replicate in most other species [1]
It is highly pathogenic in humans, HIV-1 cannot replicate in most other species [1]
A pathogen can be restricted by the presence of dominant inhibitory factors. They attack the incoming virus directly and block its integration into the host genome. This situation pertains to HIV-1 in mouse cells and represents true "intracellular immunity." Importantly, this host response is more rapid than either traditional innate or adaptive immunity and can prevent the establishment of the infection
Summary
It is highly pathogenic in humans, HIV-1 cannot replicate in most other species [1]. APOBEC proteins block the movement of some mobile genetic elements, most likely in germ cells and during embryogenesis, in mammals Besides these predominant blocks to viral replication in cells, additional barriers have been described at levels of transcription and RNA stability, as well as assembly of progeny virions. One could try to block interactions between Vif and APOBEC proteins and TASK1 and Vpu. For example, would increased levels of APOBEC3G cause editing of genomic DNA during replication, facilitating oncogenic transformation? By studying their structures, one could design inhibitors for their protein-protein interactions All these processes can be targeted by gene therapy, by introducing into cells their counterparts from different species and/or by changing binding surfaces of the host proteins so that they no longer interact with Vif or Vpu, for example. If not practical clinically, such genetic manipulation would yield important clues as to which restriction should be targeted by other therapeutic means
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