Immunoinformatics Identification of the Conserved and Cross-Reactive T-Cell Epitopes of SARS-CoV-2 with Human Common Cold Coronaviruses, SARS-CoV, MERS-CoV and Live Attenuated Vaccines Presented by HLA Alleles of Indonesian Population.

Reports on T-cell cross-reactivity against SARS-CoV-2 epitopes in unexposed individuals have been linked with prior exposure to the human common cold coronaviruses (HCCCs). Several studies suggested that cross-reactive T-cells response to live attenuated vaccines (LAVs) such as BCG (Bacillus Calmette-Guérin), OPV (Oral Polio Vaccine), and MMR (measles, mumps, and rubella) can limit the development and severity of COVID-19. This study aims to identify potential cross-reactivity between SARS-CoV-2, HCCCs, and LAVs in the context of T-cell epitopes peptides presented by HLA (Human Leukocyte Antigen) alleles of the Indonesian population.

A System Based-Approach to Examine Cytokine Response in Poxvirus-Infected Macrophages.

The poxviruses are large, linear, double-stranded DNA viruses about 130 to 230 kbp, that have an animal origin and evolved to infect a wide host range. Variola virus (VARV), the causative agent of smallpox, is a poxvirus that infects only humans, but other poxviruses such as monkey poxvirus and cowpox virus (CPXV) have crossed over from animals to infect humans. Therefore understanding the biology of poxviruses can devise antiviral strategies to prevent these human infections.

Lovastatin treatment mitigates the pro-inflammatory cytokine response in respiratory syncytial virus infected macrophage cells.

Disease severity following respiratory syncytial virus (RSV) infection is associated with inflammation due to enhanced pro-inflammatory cytokine secretion, and lung macrophage cells play a role in this process. In this study we evaluated the hydroxymethylglutaryl coenzyme A reductase inhibitor lovastatin as an anti-inflammatory drug to control RSV-induced cytokine secretion in the murine RAW 264.7 (RAW) macrophage cell line and in primary murine lung macrophages.

A systems-based approach to analyse the host response in murine lung macrophages challenged with respiratory syncytial virus.

Background: Respiratory syncytial virus (RSV) is an important cause of lower respiratory tract infection in young children. The degree of disease severity is determined by the host response to infection. Lung macrophages play an important early role in the host response to infection and we have used a systems-based approach to examine the host response in RSV-infected lung-derived macrophage cells.

Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.

The host response to the low pathogenic avian influenza (LPAI) H5N2, H5N3 and H9N2 viruses were examined in A549, MDCK, and CEF cells using a systems-based approach. The H5N2 and H5N3 viruses replicated efficiently in A549 and MDCK cells, while the H9N2 virus replicated least efficiently in these cell types. However, all LPAI viruses exhibited similar and higher replication efficiencies in CEF cells.

Evidence that selective changes in the lipid composition of raft-membranes occur during respiratory syncytial virus infection.

We examined the structure of lipid-raft membranes in respiratory syncytial virus infected cells. Cholesterol depletion studies using methyl-beta-cyclodextrin suggested that membrane cholesterol was required for virus filament formation, but not inclusion bodies. In addition, virus filament formation coincided with elevated 3-hydroxy-3-methylglutaryl-coenzyme A reductase expression, suggesting an increase in requirement for endogenous cholesterol synthesis during virus assembly.

Antiviral drugs for the control of pandemic influenza virus.

In the advent of an influenza virus pandemic it is likely that the administration of antiviral drugs will be an important first line of defence against the virus. The drugs currently in use are effective against seasonal influenza virus infection, and some cases have been used in the treatment of patients infected with the avian H5N1 influenza virus. However, it is becoming clear that the emergence of drug-resistant viruses will potentially be a major problem in the future efforts to control influenza virus infection.