Abstract
So far, only two retroviruses, human immunodeficiency virus (HIV) (type 1 and 2) and human T-cell lymphotropic virus type 1 (HTLV-1), have been recognized as pathogenic for humans. Both viruses mainly infect CD4+ T lymphocytes. HIV replication induces the apoptosis of CD4 lymphocytes, leading to the development of acquired immunodeficiency syndrome (AIDS). After a long clinical latency period, HTLV-1 can transform lymphocytes, with subsequent uncontrolled proliferation and the manifestation of a disease called adult T-cell leukemia (ATLL). Certain infected patients develop neurological autoimmune disorder called HTLV-1-associated myelopathy, also known as tropical spastic paraparesis (HAM/TSP). Both viruses are transmitted between individuals via blood transfusion, tissue/organ transplantation, breastfeeding, and sexual intercourse. Within the host, these viruses can spread utilizing either cell-free or cell-to-cell modes of transmission. In this review, we discuss the mechanisms and importance of each mode of transmission for the biology of HIV-1 and HTLV-1.
Highlights
Cell and Gene Technology Group, Institute of Gene Biology RAS, 119334 Moscow, Russia; Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Institute of Gene Biology RAS, Abstract: So far, only two retroviruses, human immunodeficiency virus (HIV) and human T-cell lymphotropic virus type 1 (HTLV-1), have been recognized as pathogenic for humans
HIV-1 and HTLV-1 viral particles have a spherical shape with a diameter of 80–100 nm, and are covered with a bilayer lipid membrane originating from the plasma membrane of an infected cell during the assembly and release of virions (Figure 1)
We previously developed the intron-regulated reporter vectors, HTLV-1 inLuc and HIV-1 inLuc, as well as HTLV-1 inYFP and HIV-1 inYFP
Summary
HIV-1 and HTLV-1 viral particles have a spherical shape with a diameter of 80–100 nm, and are covered with a bilayer lipid membrane originating from the plasma membrane of an infected cell during the assembly and release of virions (Figure 1). Mature HIV-1 and HTLV-1 virions bind and fuse with the target cell membrane through the interaction of Env with cellular receptors. The binding of the SU subunit to the receptors causes conformational changes in Env, resulting in TMmediated fusion of the viral and cellular membranes. According to the latest observations, the intact or almost intact HIV-1 capsid is translocated into the nucleus, where the reverse transcription of gRNA is completed (reviewed in [5]). It remains unclear where HTLV-1 capsid core uncoating occurs. After viral gRNA reverse transcription, proviral DNA integrates into the transcriptionally active sites within the host chromatin
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