Table 2 MSCs in viral infection
Viral infection | Virus effects on MSCs function in viral infection | References |
|---|---|---|
EBV and CMV | These viruses-induced proliferation and IFN-γ generation from peripheral blood mononuclear cells (PBMCs) were less influenced via third-party MSCs than the response to alloantigen and that MSCs had no efficacy on the development of EBV and CMV pentamer-particular T cells. MSCs have less effective T cell reactions to EBV and CMV, which compares with their powerful immunosuppressive efficacy on alloreactive T cells | [40] |
Human CMV | CB hematopoietic progenitor cells are positively differentiated into adult CD56+ CD94+ NKG2A+ NK cells on human CMV-infectious MSCs with significant greater antiviral cytokine generation compared to NK cells expanding on non-infected MSCs | [41] |
HIV-1 | The systemic inflammatory indexes, including high amounts of pro-inflammatory cytokines, chemokines, and growth factors, were reduced via UC-MSC treatment in these immune non-responders cases | [42] |
HIV-1 | Exposed to MSCs or their MSC-CM quickly enhanced HIV-1 viral protein called p24 generation. Besides, MSCs enhanced HIV-1 LTR, targeted gene expression. MSC-interceded latency-reactivation cycle was related to the PI3K and NFκB pathways. Consequently, the pre-clinically experimented suppressors of PI3K (PX-866) and NFκB (CDDO-Me) repressed MSC-interceded HIV-1 reactivation | [43] |
HIV | HIV envelope glycoprotein Gp120 suppresses CXCL12 activated chemotaxis via decreased the expression and action of CXCR4 in monocytes, B, and T cells. Gp120 led to increasing MSC CXCR4 expression. As a result, it is possible that CCR5-knockout is helpful in HIV infection treatment | [44] |
Parvovirus B19 | This virus persists in BM-MSCs of some immunocompetent persons many years afterward the first viral infection. Also, it led to enhancing the expression amounts of interleukin-6 and TNF-alpha severally and reduced BFU-E and CFU-E numeration | [76] |
HBV | Plasmapheresis and UC-MSCs transplantation are used in the therapy of HBV-dependent ACLF. The results of this treatment method were negative and unsuccessful | [47] |
Influenza virus | MSC-EVs suppressed the hemagglutination function of swine, human, and avian influenza viral about condensations of 1.25–5 μg/ml and repressed viral-caused apoptosis in lung epithelial cells of a pig | [49] |