Inhibition of Viral Membrane Fusion by Peptides and Approaches to Peptide Design

Fusion of lipid-enveloped viruses with the cellular plasma membrane or the endosome membrane is mediated by viral envelope proteins that undergo large conformational changes following binding to receptors. The HIV-1 fusion protein gp41 undergoes a transition into a “six-helix bundle” after binding of the surface protein gp120 to the CD4 receptor and a co-receptor. Synthetic peptides that mimic part of this structure interfere with the formation of the helix structure and inhibit membrane fusion. This approach also works with the S spike protein of SARS-CoV-2. Here we review the peptide inhibitors of membrane fusion involved in infection by influenza virus, HIV-1, MERS and SARS coronaviruses, hepatitis viruses, paramyxoviruses, flaviviruses, herpesviruses and filoviruses. We also describe recent computational methods used for the identification of peptide sequences that can interact strongly with protein interfaces, with special emphasis on SARS-CoV-2, using the PePI-Covid19 database.

A Review of Infectious Diseases Associated with Religious and Nonreligious Rituals

Rituals are an integral part of human life but a wide range of rituals (both religious and non-religious), from self-flagellation to blood brotherhood to ritual sprinkling of holy water, have been associated with transmission of infections. These infections include angiostrongyliasis, anthrax, brucellosis, cholera, COVID-19, cutaneous larva migrans, Ebola, hepatitis viruses, herpes simplex virus, HIV, human T-cell leukemia virus (HTLV), kuru, Mycobacterium bovis, Naegleria fowleri meningoencephalitis, orf, rift valley fever, and sporotrichosis. Education and community engagement are important cornerstones in mitigating infectious risks associated with rituals.

Host Innate Immunity Against Hepatitis Viruses and Viral Immune Evasion

Hepatitis viruses are primary causative agents of hepatitis and represent a major source of public health problems in the world. The host innate immune system forms the first line of defense against hepatitis viruses. Hepatitis viruses are sensed by specific pathogen recognition receptors (PRRs) that subsequently trigger the innate immune response and interferon (IFN) production. However, hepatitis viruses evade host immune surveillance via multiple strategies, which help compromise the innate immune response and create a favorable environment for viral replication. Therefore, this article reviews published findings regarding host innate immune sensing and response against hepatitis viruses. Furthermore, we also focus on how hepatitis viruses abrogate the antiviral effects of the host innate immune system.

Basic reproduction numbers of three strains of mouse hepatitis viruses in mice

Mouse hepatitis virus (MHV) is a murine coronavirus and one of the most important pathogens in laboratory mice. Although various strains of MHV have been isolated, they are generally excreted in the feces and transmitted oronasally via aerosols and contaminated bedding. In this study, we attempted to determine the basic reproduction numbers of three strains of MHV to improve our understanding of MHV infections in mice. Five-week-old female C57BL/6J mice were inoculated intranasally with either the Y, NuU, or JHM variant strain of MHV and housed with two naive mice. After 4 weeks, the presence or absence of anti-MHV antibody in the mice was determined by the enzyme-linked immunosorbent assay. We also examined the distribution of MHV in the organs of Y, NuU, or JHM variant-infected mice. Our data suggest that the transmissibility of MHV is correlated with viral growth in the gastrointestinal tract of infected mice. To the best of our knowledge, this is the first report to address the basic reproduction numbers among pathogens in laboratory animals.

COVID-19 with acute hepatitis A virus co-infection in a fully-vaccinated individual: a case report

In a developing country with varying degree of public hygiene and sanitation, prevalent infectious diseases such as hepatitis A (HAV) could add to the burden of infection during coronavirus disease 2019 (COVID-19) pandemic and complicate its gastrointestinal and hepatic manifestation. Here we present a case COVID-19 with acute hepatitis A virus co-infection in a young female with fever, joint pain, non-productive cough, loss of smell, abdominal discomfort, darkened urine, and pale loose stool before admission. The significant finding was slightly icteric sclera, hepatomegaly with tenderness in the epigastrium and right upper quadrant, increase in aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, C-reactive protein and, D-dimer. A naso-oropharyngeal swab examination for SARS-CoV-2 infection was positive, and IgM anti-HAV was reactive with a total anti-HAV titer 60 mIU/mL. Subsequently, she was hospitalized for 14 days, successfully recovered; her symptoms resolved and her level of liver enzymes back to normal, and she was discharged for self-isolation at home. RT-PCR for SARS-CoV-2 infection came back negative 7 days later. In light of the pandemic, physicians need to raise suspicion of co-infection of COVID-19 with other hepatitis viruses in cases with gastrointestinal and hepatic manifestation. A marked increase in liver enzyme may warrant further testing for hepatitis viruses where such infection should be suspected.

Sex Differences in Immunity to Viral Infections

The ongoing COVID-19 pandemic has increased awareness about sex-specific differences in immunity and outcomes following SARS-CoV-2 infection. Strong evidence of a male bias in COVID-19 disease severity is hypothesized to be mediated by sex differential immune responses against SARS-CoV-2. This hypothesis is based on data from other viral infections, including influenza viruses, HIV, hepatitis viruses, and others that have demonstrated sex-specific immunity to viral infections. Although males are more susceptible to most viral infections, females possess immunological features that render them more vulnerable to distinct immune-related disease outcomes. Both sex chromosome complement and related genes as well as sex steroids play important roles in mediating the development of sex differences in immunity to viral infections.