SARS-CoV-2 has spread very quickly from its first reported case on 19 January 2020 in the United Stated of America, leading WHO to declare pandemic by 11 March 2020. RNA viruses accumulate mutations following replication and passage in human population, which prompted us to determine the rate and the regions (hotspots) of the viral genome with high rates of mutation. We analyzed the rate of mutation accumulation over a period of 11 weeks (submitted between 19th January to 15 April 2020) in USA SARS-CoV-2 genome. Our analysis identified that majority of the viral genes accumulated mutations, although with varying rates and these included NSP2, NSP3, RdRp, helicase, Spike, ORF3a, ORF8, and Nucleocapsid protein. Sixteen mutations accumulated in Spike protein in which four mutations are located in the receptor binding domain. Intriguingly, we identified a fair number of viral proteins (NSP7, NSP9, NSP10, NSP11, Envelop, ORF6, and ORF7b proteins), which did not accumulate any mutation. Limited changes in these proteins may suggest that they have conserved functions, which are essential for virus propagation. This provides a basis for a better understanding of the genetic variation in SARS-CoV-2 circulating in the US, which could help in identifying potential therapeutic targets for controlling COVID-19.

Multiple sclerosis (MS) is an immune inflammatory disease, where the underlying etiological cause remains elusive. Multiple triggering factors have been suggested, including environmental, genetic and gender components. However, underlying infectious triggers to the disease are also suspected. There is an increasing abundance of evidence supporting a viral etiology to MS, including the efficacy of interferon therapy and over-detection of viral antibodies and nucleic acids when compared with healthy patients. Several viruses have been proposed as potential triggering agents, including Epstein–Barr virus, human herpesvirus 6, varicella–zoster virus, cytomegalovirus, John Cunningham virus and human endogenous retroviruses. These viruses are all near ubiquitous and have a high prevalence in adult populations (or in the case of the retroviruses are actually part of the genome). They can establish lifelong infections with periods of reactivation, which may be linked to the relapsing nature of MS. In this review, the evidence for a role for viral infection in MS will be discussed with an emphasis on immune system activation related to MS disease pathogenesis.

The newly identified pathogenic human coronavirus, SARS-CoV-2, led to an atypical pneumonia-like severe acute respiratory syndrome (SARS) outbreak called coronavirus disease 2019 (abbreviated as COVID-19). Currently, nearly 77 million cases have been confirmed worldwide with the highest numbers of COVID-19 cases in the United States. Individuals are getting vaccinated with recently approved vaccines, which are highly protective in suppressing COVID-19 symptoms but there will be a long way before the majority of individuals get vaccinated. In the meantime, safety precautions and effective disease control strategies appear to be vital for preventing the virus spread in public places. Due to the longevity of the virus on smooth surfaces, photocatalytic properties of “self-disinfecting/cleaning” surfaces appear to be a promising tool to help guide disinfection policies for controlling SARS-CoV-2 spread in high-traffic areas such as hospitals, grocery stores, airports, schools, and stadiums. Here, we explored the photocatalytic properties of nanosized TiO2 (TNPs) as induced by the UV radiation, towards virus deactivation. Our preliminary results using a close genetic relative of SAR-CoV-2, HCoV-NL63, showed the virucidal efficacy of photoactive TNPs deposited on glass coverslips, as examined by quantitative RT-qPCR and virus infectivity assays. Efforts to extrapolate the underlying concepts described in this study to SARS-CoV-2 are currently underway.

Two clinical syndromes are associated with hantavirus infection in humans: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Autopsy findings typically reveal a common feature of increased permeability in microvascular beds, suggesting vascular endothelium is a prime target for virus infection. Endothelial cells are susceptible to hantavirus infection; however, virus does not cause cytopathic effects, to explain increased endothelium permeability. Therefore, immune mechanisms were suggested to play a crucial role in hantavirus pathogenesis. In this review, we summarize data on hantavirus-induced immune disturbances and discuss their implication in capillary leakage caused by hantavirus infection.