EG.5 (Eris) and BA.2.86 (Pirola) two new subvariants of SARS-CoV-2: a new face of old COVID-19.

BACKGROUND: The World Health Organization announced the end of the Coronavirus Disease of 2019 (COVID-19) global health emergency on May 5, 2023. However, the reports from different countries indicate an elevation in the number of COVID-19-related hospitalizations and deaths through the last months. The subvariant XBB.1.5 (Kraken) was the cause of 49.1% of COVID-19 cases by the end of January 2023. Although, the subvariant EG.5 (Eris) has surpassed the XBB.1.5 recently. EG.5 is a close subvariant descending from XBB.1.9.2 subvariant of Omicron. EG.5.1 is a sublineage carrying two crucial spike mutations F456L and Q52H. Up to now, it is not well-established whether its infectivity, severity, and immune evasion have shown any change or not. Also, BA.2.86 another subvariant of Omicron descending from BA.2 bears over 30 mutations which could affect its infectivity and transmissibility. METHODS: Scopus, PubMed, Google Scholar, and Google were searched with six keywords up to 20 November 2023 and highly reliable research and reports were selected to refer to in this article. PURPOSE: This brief review aims to overview the most reliable data about EG.5 and BA.2.86 based on scientific evidence. CONCLUSION: Based on the currently available data these two new subvariants have similar features with currently circulating variants of Omicron and are less immune evasive than ancestral SARS-CoV-2.

Targeting the cGAS-STING pathway as an inflammatory crossroad in coronavirus disease 2019 (COVID-19).

CONTEXT AND OBJECTIVE: The emerging pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has imposed significant mortality and morbidity on the world. An appropriate immune response is necessary to inhibit SARS-CoV-2 spread throughout the body. RESULTS: During the early stages of infection, the pathway of stimulators of interferon genes (STING), known as the cGAS-STING pathway, has a significant role in the induction of the antiviral immune response by regulating nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Interferon regulatory factor 3 (IRF3), two key pathways responsible for proinflammatory cytokines and type I IFN secretion, respectively. DISCUSSION: During the late stages of COVID-19, the uncontrolled inflammatory responses, also known as cytokine storm, lead to the progression of the disease and poor prognosis. Hyperactivity of STING, leading to elevated titers of proinflammatory cytokines, including Interleukin-I (IL-1), IL-4, IL-6, IL-18, and tissue necrosis factor-α (TNF-α), is considered one of the primary mechanisms contributing to the cytokine storm in COVID-19. CONCLUSION: Exploring the underlying molecular processes involved in dysregulated inflammation can bring up novel anti-COVID-19 therapeutic options. In this article, we aim to discuss the role and current studies targeting the cGAS/STING signaling pathway in both early and late stages of COVID-19 and COVID-19-related complications and the therapeutic potential of STING agonists/antagonists. Furthermore, STING agonists have been discussed as a vaccine adjuvant to induce a potent and persistent immune response.