寄生虫逃避免疫功能不全宿主

Abstract

Parasites can increase infection rates and pathogenicity in immunocompromised human immunodeficiency virus (HIV) patients. However, in vitro studies and epidemiological investigations also suggest that parasites might escape immunocompromised hosts during HIV infection. Due to the lack of direct evidence from animal experiments, the effects of parasitic infections on immunocompromised hosts remain unclear. Here, we detected 14 different parasites in six northern pig-tailed macaques (NPMs) before or at the 50th week of simian immunodeficiency virus (SIV) infection by ELISA. The NPMs all carried parasites before viral injection. At the 50th week after viral injection, the individuals with negative results in parasitic detection (i.e., 08247 and 08287) were characterized as the Parasites Exit (PE) group, with the other individuals (i.e., 09203, 09211, 10205, and 10225) characterized as the Parasites Remain (PR) group. Compared with the PR group, the NPMs in the PE group showed higher viral loads, lower CD4+ T cells counts, and lower CD4/CD8 rates. Additionally, the PE group had higher immune activation and immune exhaustion of both CD4+ and CD8+ T cells. Pathological observation showed greater injury to the liver, cecum, colon, spleen, and mesenteric lymph nodes in the PE group. This study showed more seriously compromised immunity in the PE group, strongly indicating that parasites might exit an immunocompromised host.

Successful implementation of intestinal resection and anastomosis in non-human primates suggests the possibility of longitudinal intestinal research

“…In addition, approximately 60%–80% of memory CD4 + T cells in the gastrointestinal tract are depleted within days of HIV and simian immunodeficiency virus (SIV) infection ( Veazey, 2019 ). Both HIV/SIV infections are also associated with structural and functional impairment of gut mucosal tissue ( Song et al, 2018 ; Zhang et al, 2016; Zhang et al, 2019 ). For instance, during infection, intestinal villi become flat and sucrase activity is reduced ( Brenchley & Douek, 2008 ), with disruption of the intestinal epithelial barrier leading to microbial translocation and chronic immune activation ( Somsouk et al, 2015 ), which can further accelerate and exacerbate HIV infection.…”