Free radical release due to oxidative stress is gaining importance in the field of viral pathogenesis. Recent studies suggest the involvement of oxidative stress and ROS levels in regulating disease virulence during RNA virus infection. Most of the RNA virus infections lead to vascular dysfunction and disease severity. However, the biology of free radicals in maintaining vascular endothelium integrity is not completely understood. In the present review, we discuss some of the common features in positive-strand RNA virus infections such as dengue and SARS-CoV-2 and suggest that anti-oxidant therapy could pave the way to develop therapeutic strategies in combating emerging and re-emerging RNA viruses. Supplementary Information The online version contains supplementary material available at 10.1007/s12192-022-01269-x.

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Endothelial dysfunction is one of the key cornerstone complications of emerging and re-emerging viruses which lead to vascular leakage and a high mortality rate. The mechanism that regulates the origin of endothelial dysregulation is not completely elucidated. Currently, there are no potential pharmacological treatments and curable management for such diseases. In this sense, mesenchymal stromal/stem cells (MSCs) has been emerging to be a promising therapeutic strategy in restoring endothelial barrier function in various lung disease, including ALI and ARDS. The mechanism of the role of MSCs in restoring endothelial integrity among single-strand RNA (ssRNA) viruses that target endothelial cells remains elusive. Thus, we have discussed the therapeutic role of MSCs in restoring vascular integrity by (i) inhibiting the metalloprotease activity thereby preventing the cleavage of tight junction proteins, which are essential for maintaining membrane integrity (ii) possessing antioxidant properties which neutralize the excessive ROS production due to virus infection and its associated hyper host immune response (iii) modulating micro RNAs that regulate the endothelial activation and its integrity by downregulating the inflammatory response during ssRNA infection.

Background It is reported that cancer patients are more susceptible to SARS-CoV-2 infection due to immunocompromised immunity. To understand the long-term impact of SARS-CoV-2 in HNSC cancer, the current study is designed to assess the status of two vital host molecules (ACE2 & TMPRSS2) for the entry of virus in HNSC patients using computational methods. Methodology We used public databases such as TIMER, UALCAN, and GEPIA2 to assess the mRNA expression and association of ACE2 and TMPRSS2 in HNSC. cBioPortal was used to assess the genetic alterations in the ACE2 and TMPRSS2 protein sequences that are involved in HNSC development. The CTD database was also used to identify the genes associated with COVID-19 and HNSC. Finally, the PANTHER online platform was used to investigate the protein-protein interaction between COVID-19 and HNSC progression genes collected from the CTD database. Results A differential expression of ACE2 (downregulated) and TMPRSS2 (upregulated) was noted in HNSC those with human papilloma viral infections. A strong genetic alteration in the protein sequence of ACE2 and TMPRSS2 supports their significant role in HNSC disease progression. In addition, the protein-protein interaction network revealed that genes associated with COVID-19 and HNSC are strongly involved in binding activity, catalytic activity, and various cancer signaling pathways. Conclusion From our in silico analysis, we would like to conclude that ACE2 and TMPRSS2 are strongly associated with disease progression in both pathological conditions (HNSC and COVID-19). So, it could serve as potential biomarkers for the early prediction of disease outcomes in cancer patients with COVID-19 disease. Thus, further investigation is needed to evaluate the long-term impact of SARS-CoV-2 infection on HNSC patients.

BackgroundPlasma leakage due to endothelial permeability is regarded as a hallmark process in the pathophysiology of severe dengue. In recent years, the importance of ceramide in regulating vascular tone during viral infection and metabolic diseases has gained attention. The present study aimed to evaluate the plasma levels of ceramide and its association with plasma leakage in dengue patients.MethodsThe study involved 30 dengue samples involving severe dengue (SD-10), Dengue with Warning sign (DWW-10), Dengue without Warning Sign (DWOW-10), along with other febrile illness (OFI-10) controls. Samples were collected on the day of admission (DOA), day of defervescence (DOD), and day of convalescence (DOC). Total plasma ceramides (d18:1/22:0) were quantified using RP-HPLC. The correlation between ceramides and hematocrit/platelet count was evaluated using Spearman Rho Correlation. All the statistical analyses were performed using SPSS software.ResultsDuring the febrile phase, a significant (P≤0.05) decrease in the levels of ceramides was observed in dengue compared to OFI (control). Towards the defervescences, the ceramides levels were substantially (P ≤ 0.001) elevated in dengue groups compared to baseline. Most importantly, the ceramide levels were found to be higher in SD patients compared to non-severe dengue (DWW & DWOW) and OFI, particularly at the critical phase of infection. We observed a significant negative correlation (r = -0.867, P ≤0.001) between the platelet count and ceramide levels in SD subjects. Notably, a negative correlation was observed between ceramide and hematocrit during the defervescence phase (R = -0.355, P≤0.05) in the AD group.ConclusionElevated levels of circulating plasma ceramides during the defervescence phase of severe dengue show an essential role of ceramides in disease pathogenesis, however further studies are required to ascertain it.