Oral epithelial cells and their interactions with HIV‐1

Abstract

As the AIDS pandemic has continued, our understanding of the events that occur during the entry and infection of conventional, susceptible cells has increased dramatically, leading to the development of control therapies for HIV‐infected individuals. However, an ongoing hole in our understanding is how HIV crosses the mucosal barriers to gain access to permissive cells, despite how important this information would be in developing successful vaccines and other preventative measures such as topical anti‐HIV microbicides. In particular, our knowledge of the role that epithelial cells of the mucosal surfaces play in infection – both during early phases and throughout the life of an infected individual, is currently hazy at best. However, several studies in recent years suggest that HIV can bind to and traverse these mucosal epithelial cells, providing a reservoir of infection that can subsequently infect underlying permissive cells. Despite this interaction with epithelial cells, evidence suggests HIV‐1 does not productively infect these cells, although they are capable of transferring surface‐bound and transcytosed virus to other, permissive cells. Further, there appear to be key differences between adult and infant epithelial cells in the degree to which HIV can transcytose and infect the epithelium. Thus, it is clear that, whilst not primary targets for infection and virus replication, epithelial cells play an important role in the infection cycle and improving our understanding of their interactions with HIV could potentially provide key insights necessary to develop effective preventative therapies.

Novel viruses detected in bats in the Republic of Korea

“…Additionally, as a result of verification by PCR in individual samples, the viruses were not only found in pooled tissue samples, including the brain, lung, intestine, and liver, but also oral swabs. Recent studies suggest that RV can bind to and traverse mucosal epithelial cells, and the epithelial cells play an important role in the infection cycle, although they are not targets for viral infection and replication 35 . This indicates that retroviruses can be detected in bat oral swabs, as in the results of the present study.…”

Human immunodeficiency virus interaction with oral and genital mucosal epithelia may lead to epithelial–mesenchymal transition and sequestration of virions in the endosomal compartments

“…HIV‐1 intra‐epithelial sequestration without substantial HIV‐1 release is common in tonsil, cervical, and foreskin epithelial cells isolated from different donors (Yasen et al., 2017, 2018), suggesting that this phenomenon may be relevant to the biological functions of both oral and genital mucosal epithelia. Although these epithelia are found at different anatomical sites, they have similar morphological features—squamous epithelial morphology and stratified organization—and serve as portals of entry for HIV‐1 (Bouschbacher et al., 2008; Carias et al., 2013; Dinh et al., 2015; Tugizov et al., 2011, 2012; Zhou et al., 2011) (Kohli et al., 2014; Moyes, Islam, Kohli, & Naglik, 2016). Squamous epithelia from different anatomical locations may also have similar mechanisms for HIV‐1 sequestration in their endosomal/vesicular compartments (Yasen et al., 2017, 2018).…”

HIV Infection and Oral Manifestations: An Update

“…In summary, HIV replication occurs when the heterodimer proteins gp120 and gp41 of the viral envelope bind to proteins in the cell membrane of target cells; that is, gp120 binds to CD4 monomeric glycoprotein on the cell surface of T lymphocytes or precursor T cells of lymphatic tissues such as bone marrow and thymus, macrophages, eosinophils, dendritic cells, and microglial cells [2,21,[37][38][39] and after that, viral RNA is released inside the cells and tissues that will follow its cycle replication from the early stages of infection can be intensely active, as well as allowing the establishment of a latent infection, particularly known as permanent viral reservoirs promoting a major obstacle in the complete eradication of HIV infection and effectiveness in antiretroviral treatment [40][41][42][43][44].…”