Table 3.
Examples of viruses targeting MSCs and related pathologies.
| Cells | Viruses | Related Outcomes |
|---|---|---|
| Bone marrow-MSC | HIV | Inability to support Hematopoietic Stem Cells expansion and implication in HIV-related cytopenia [27]; HIV-related reactivation [187,188,189] |
| HCMV | Transmit to neighboring cells after reactivation [190,191] | |
| Modifies the physiological interaction between BM-MSCs and HSC | ||
| Impairment of osteoblast regeneration, cartilage regeneration, hematopoiesis and properties of immune progenitor cells [191] | ||
| HHV | Lower proliferation rates and altered phenotypes related to malignant transformation [190,192,193] | |
| Influenza A H5N1 | Risk of transmission during bone marrow transplantation [194,195] | |
| RSV | Alteration of immunoregulatory functions [196] | |
| ZIKV | Impaired osteoblast differentiation and possible implication in development of bone pathologies [197] | |
| HBV | HBV-associated myocarditis and other HBV-related extrahepatic diseases [198] | |
| Lung resident MSC/pericytes | SARS-CoV-2 | Pericyte apoptosis and loss in COVID-19 patients [199,200] |
| SIV/HIV | Development of HIV-related pulmonary complications [197,201] | |
| Hepatic Stellate Cell (HepSC, Ito cells) | HIV | HepSC activation and chemotaxis through HIV gp120 envelope protein [202,203] |
| HCV | HCV proteins as well as RNA released by hepatocytes are activating HepSC [204,205]. Constant activation leading to liver fibrosis [206,207,208,209] | |
| HBV | Release of IL-17 by infected cells which stimulate liver fibrosis by activation of HepSC [210,211]. | |
| Mesangial Cell (Kidney) | HIV | HIV-associated glomerulosclerosis due to increased proliferation and matrix synthesis [212,213] |
| HCMV | Glomerulosclerosis [214,215,216,217] | |
| HCV | Glomerulonephritis [218] | |
| ZIKV | Viral reservoir (persistent viruria) [219] | |
| SARS-CoV-2 | Stromal (MSC-like cells) are infected and may contribute to kidney fibrosis in a model of spheroid cultures and to be correlated with kidney fibrosis in COVID19 patients [220]. | |
| Brain Pericytes (BP) | HIV | Decreased BPs coverage of blood brain barrier (BBB) associated with higher permeability [221,222] |
| IL-6 and PDGF-BB secretions concur in HIV-induced CNS damage and BBB disruption [221,223] | ||
| HCMV | Contribute to HCMV dissemination [224] | |
| CXCL8, CXCL11, CCL5, TNF-α, IL-1β and IL-6 secretion causing neuroinflammation [225] | ||
| JEV | IL-6 secretion leads to ZO-1 degradation and BBB impairment [226] | |
| PGE2 and RANTES secretion by BPs recruit leukocytes to the site of infection. Associated with BBB impairment, this provoke leukocyte infiltration and major neuroinflammation [227] | ||
| HSV | BBB impairment associated with leukocytes recruitment leading to major neuroinflammation [228] | |
| ZIKV | Brain abnormalities and BBB defect [229,230] | |
| Osteoblasts | HIV (gp120) | TNF-α and impaired Wnt/β-Catenin signaling promote bone demineralization and reduced bone mass leading to osteopenia and osteoprosis [231] |
| RRV | Imbalance in RANKL/OPG ratio in favor of osteoclastogenic activities and bone loss [232,233] | |
| CHIKV | Proinflammatory (IL-6) and pro-osteoclastic (RANKL) effects in infected cells [234] | |
| HCV | Associated with bone density hardening and osteosclerosis [235] | |
| Increased risk of osteoporosis [236] | ||
| Increased risk of fracture [237] | ||
| Impairment of RANKL/OPG ratio [235] | ||
| ZIKV | Impaired osteoblasts function triggering an imbalance in bone homeostasis and inducing bone-related disorders [197] | |
| MeV | Higher expression of several osteogenic markers and osteogenic differentiation [238] | |
| Otosclerosis [239] | ||
| Paget’s disease [240] | ||
| Schwann Cell (SC) | HIV | Dorsal root ganglion neurotoxicity, including axon and myelin injury [241] |
| HSV/VZV | The principal mechanism evoked for HSV-induced GBS is a molecular mimicry of viral proteins [242] | |
| HCMV | Probable molecular mimicry generating autoantibodies against moesin expressed by SCs [243,244,245,246,247] | |
| ZIKV | Possible direct viral pathogenic effect or a cell-mediated inflammation in pathogenesis of ZIKV-associated GBS [248] | |