Maksoud Semer, El Hokayem Joelle
Experimental Therapeutics and Molecular Imaging Unit, Department of Neurology, Neuro-Oncology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, United States.
Heliyon. 2023 Apr 1;9(4):e15055. doi: 10.1016/j.heliyon.2023.e15055. eCollection 2023 Apr.
HIV infection progressively weakens the immune system by infecting and destroying cells involved in host defense. Viral infection symptoms are generated and aggravated as immunosuppression progresses, triggered by the presence of opportunistic infections: among these is leishmaniasis, a disease caused by the intracellular parasite . The incidence of this co-infection is growing progressively due to the geographic distribution overlap. Both pathogens infect monocytes/macrophages and dendritic cells, although they can also modulate the activity of other cells without co-infecting, such as T and B lymphocytes. /HIV co-infection could be described as a system comprising modulations of cell surface molecule expression, production of soluble factors, and intracellular death activities, leading ultimately to the potentiation of infectivity, replication, and spread of both pathogens. This review describes the cytokine/chemokine response in /HIV infection and co-infection, discussing how these molecules modulate the course of the disease and analyzing the therapeutic potential of targeting this network.
人类免疫缺陷病毒(HIV)感染通过感染和破坏参与宿主防御的细胞,逐渐削弱免疫系统。随着免疫抑制的进展,机会性感染的出现引发并加重了病毒感染症状:其中包括利什曼病,一种由细胞内寄生虫引起的疾病。由于地理分布重叠,这种合并感染的发生率正在逐渐上升。两种病原体都感染单核细胞/巨噬细胞和树突状细胞,尽管它们也可以在不合并感染的情况下调节其他细胞的活性,如T和B淋巴细胞。HIV合并感染可被描述为一个系统,包括细胞表面分子表达的调节、可溶性因子的产生以及细胞内死亡活动,最终导致两种病原体的传染性、复制和传播增强。本综述描述了HIV感染和合并感染中的细胞因子/趋化因子反应,讨论了这些分子如何调节疾病进程,并分析了针对该网络的治疗潜力。