Sibeko Sengeziwe, Sanderson Micheline, Moyo Sizulu, Botha Matthys H
Public Health, Societies and Belonging Division, Human Sciences Research Council, Durban, South Africa.
Division of Anatomical Pathology, Department of Pathology, Stellenbosch University, Cape Town, South Africa.
Front Reprod Health. 2024 May 2;6:1408198. doi: 10.3389/frph.2024.1408198. eCollection 2024.
Two-thirds of people living with human immunodeficiency virus type 1 (HIV-1) infection reside in Sub-Saharan Africa, where there are the highest prevalence and incidence rates of human papillomavirus (HPV) infection. Both infections are sexually transmitted and enter the body via the epithelium. This review describes the extent of involvement of the epithelium in each infection in the female genital tract.
A narrative review was conducted on the role of the epithelium in HPV and HIV-1 infections.
An intact epithelial barrier is the predominant form of protection against viral entry and infection, including from HIV-1 and HPV. HPV is an intraepithelial pathogen, and thus, its growth and amplification, which are dependent on squamous cell differentiation, occur in the epithelium. It gains entry to the basal cells of the stratified squamous epithelium via micro-abrasions or other epithelial injuries that expose the basement membrane. HIV-1, conversely, passes through the epithelium to infect subepithelial tissues. Following deposition of the HIV-1-containing inoculum into the lumen, the virus enters the mucosa through breaks in the epithelial barrier within hours of infection. Further, HIV-1 penetrates the epithelium via various mechanisms, including paracellular passage or across epithelial cells through transcytosis. The capture of the virus from the mucosal surface by intraepithelial and/or subepithelial target cells has also been documented.
Epithelial disruption is the major pathogenetic pathway in HIV-1 and HPV infections. Therefore, biochemical compounds that strengthen the epithelial barrier must be prioritized to prevent these infections.
三分之二的1型人类免疫缺陷病毒（HIV-1）感染者居住在撒哈拉以南非洲，该地区人乳头瘤病毒（HPV）感染的患病率和发病率最高。这两种感染均通过性传播，并经上皮进入人体。本综述描述了上皮在女性生殖道每种感染中的受累程度。
对上皮在HPV和HIV-1感染中的作用进行叙述性综述。
完整的上皮屏障是防止病毒进入和感染（包括HIV-1和HPV）的主要保护形式。HPV是一种上皮内病原体，因此其生长和扩增依赖于鳞状细胞分化，发生在上皮内。它通过微擦伤或其他暴露基底膜的上皮损伤进入复层鳞状上皮的基底细胞。相反，HIV-1穿过上皮感染上皮下组织。在将含有HIV-1的接种物沉积到管腔后，病毒在感染后数小时内通过上皮屏障的破损处进入黏膜。此外，HIV-1通过多种机制穿透上皮，包括细胞旁途径或通过转胞吞作用穿过上皮细胞。上皮内和/或上皮下靶细胞从黏膜表面捕获病毒的现象也有记录。
上皮破坏是HIV-1和HPV感染的主要致病途径。因此，必须优先考虑增强上皮屏障的生化化合物以预防这些感染。
