The cytokine/chemokine response in Leishmania/HIV infection and co-infection. Issue 4 (April 2023)

• Record Type: Journal Article
• Authors: Maksoud, Semer; El Hokayem, Joelle
• Is Part Of: Heliyon. Volume 9:Issue 4(2023)
• Publication Date: 2023-04
• Subjects: Leishmania -- HIV -- Cytokine -- Chemokine -- Co-infection -- Interleukin; Research -- Periodicals; Medical sciences -- Periodicals; Natural history -- Periodicals; Social sciences -- Periodicals; Earth sciences -- Periodicals; Physical sciences -- Periodicals; 507.2
• DOI: 10.1016/j.heliyon.2023.e15055
• Languages: English
• ISSNs: 2405-8440

Abstract

Abstract: 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 Leishmania . 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. Leishmania /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 Leishmania /HIV infection and co-infection, discussing how these molecules modulate the course of the disease and analyzing the therapeutic potential of targeting this network. Highlights: Cytopathic and molecular changes exacerbate the replication and infectivity of both pathogens during co-infection. A Th1→Th2 transition of the cytokine/chemokine response during co-infection has been described. Caution should be taken when targeting cytokines/chemokines that have differential effects on these pathogens.