Background Influenza virus infection is among the most detrimental threats to the health of humans and some animals, infecting millions of people annually all around the world and in many thousands of cases giving rise to pneumonia and death. All those health crises happen despite previous and recent developments in anti-influenza vaccination, suggesting the need for employing more sophisticated methods to control this malign infection. Main body The innate immunity modules are at the forefront of combating against influenza infection in the respiratory tract, among which, innate T cells, particularly gamma-delta (γδ) T cells, play a critical role in filling the gap needed for adaptive immune cells maturation, linking the innate and adaptive immunity together. Upon infection with influenza virus, production of cytokines and chemokines including CCL3, CCL4, and CCL5 from respiratory epithelium recruits γδ T cells at the site of infection in a CCR5 receptor-dependent fashion. Next, γδ T cells become activated in response to influenza virus infection and produce large amounts of proinflammatory cytokines, especially IL-17A. Regardless of γδ T cells’ roles in triggering the adaptive arm of the immune system, they also protect the respiratory epithelium by cytolytic and non-cytolytic antiviral mechanisms, as well as by enhancing neutrophils and natural killer cells recruitment to the infection site. Conclusion In this review, we explored varied strategies of γδ T cells in defense to influenza virus infection and how they can potentially provide balanced protective immune responses against infected cells. The results may provide a potential window for the incorporation of intact or engineered γδ T cells for developing novel antiviral approaches or for immunotherapeutic purposes.

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Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) emerged in December 2019 in Wuhan province, China. SARS-CoV-2 causes coronavirus disease 2019 . Angiotensin-converting enzyme 2 (ACE2) has an essential role as a receptor in the entry of the SARS-CoV-2 into the host cells. It has been declared, ACE2 expresses in the lungs, heart, kidneys, placenta, and liver. This study reviews the liver's markers' characteristics in patients with COVID-19 to achieve novel insights in improving clinical treatment. Liver disease and chronic kidney disease patients are susceptible to COVID-19. There is limited information about the effects of SARS-COV-2 on patients with preexisting liver associated disorders, including chronic hepatitis B virus or hepatitis C virus, primary biliary cirrhosis, nonalcoholic fatty liver disease, and more are yet to be understood. By considering conducted studies in this manner since ACE2 receptors, which are the primary receptors for SRAS-CoV-2, exist on the liver and lungs, heart, kidneys, and placenta, SRAS-CoV-2 can infect liver cells too. Consequently, this infection will have resulted in liver function tests' escalated levels and total bilirubin as biochemical biomarkers. Further investigations need to be done to point out the hepatic manifestations of COVID-19's infected patients with chronic liver disease and improve clinical management and more stringent preventive measures for this type of infected patients.

The severe acute respiratory syndrome (SARS-CoV-2), a newly emerging of coronavirus, continues to infect humans in the absence of a viable treatment. Neutralizing antibodies that disrupt the interaction of RBD and ACE2 has been under the spotlight as a way of developing the COVID-19 treatment. Some animals, such as llamas, manufacture heavy-chain antibodies that have a single variable domain (VHH) instead of two variable domains (VH/VL) as opposed to typical antibodies. Nanobodies are antigen-specific, single-domain, changeable segments of camelid heavy chain-only antibodies that are recombinantly produced. These types of antibodies exhibit a wide range of strong physical and chemical properties, like high solubility, and stability. The VHH's high-affinity attachment to the receptor-binding domain (RBD) allowed the neutralization of SARS-CoV-2. To tackle COVID-19, some nanobodies are being developed against SARS-CoV-2, some of which have been recently included in clinical trials. Nanobody therapy may be useful in managing the COVID-19 pandemic as a potent and low-cost treatment. This paper describes the application of nanobodies as a new class of recombinant antibodies in COVID-19 treatment.

Epstein-Barr virus (EBV)-associated gastric cancer (EBVaGC) is regarded as the most prevalent malignant tumor triggered by EBV infection. In recent years, increasing attention has been considered to recognize more about the disease process's exact mechanisms. There is accumulating evidence that showing epigenetic modifications play critical roles in the EBVaGC pathogenesis. MicroRNAs (miRNAs), as critical epigenetic modulators, are single-strand short noncoding RNA (length< 200 bp), which regulate gene expression through binding to the 3ʹ-untranslated region (3ʹ-UTR) of target RNA transcripts and either degrade or repress their activities. In the latest research on EBV, it was found that this virus could encode miRNAs. Mechanistically, EBV-encoded miRNAs are involved in carcinogenesis and the progression of EBV-associated malignancies. Moreover, these miRNAs implicated in immune evasion, identification of pattern recognition receptors, regulation of lymphocyte activation and lethality, modulation of infected host cell antigen, maintain of EBV infection status, promotion of cell proliferation, invasion and migration, and reduction of apoptosis. As good news, not only has recent data demonstrated the crucial function of EBV-encoded miRNAs in the pathogenesis of EBVaGC, but it has also been revealed that aberrant expression of exosomal miRNAs in EBVaGC has made them biomarkers for detection of EBVaGC. Regarding these substantial characterizes, the critical role of EBV-encoded miRNAs has been a hot topic in research. In this review, we will focus on the multiple mechanisms involved in EBVaGC caused by EBV-encoded miRNAs and briefly discuss their potential application in the clinic as a diagnostic biomarker.

The SARS‐coronavirus‐2 (SARS‐CoV‐2) that causes coronavirus disease 2019 (COVID‐19), has spread worldwide and caused a global health emergency. SARS‐CoV‐2 is a coronaviridae virus that infects target cells by interacting with the plasma membrane‐expressed angiotensin‐converting enzyme 2 (ACE2) via the S1 component of the S protein. Effective host immune response to SARS‐CoV‐2 infection, which includes both innate and adaptive immunity, is critical for virus management and elimination. The intensity and outcome of COVID‐19 may be related to an overabundance of pro‐inflammatory cytokines, which results in a “cytokine storm” and acute respiratory distress syndrome. After SARS‐CoV‐2 infection, the immune system's hyperactivity and production of autoantibodies may result in autoimmune diseases such as autoimmune hemolytic anemia, autoimmune thrombocytopenia, Guillain‐Barré syndrome, vasculitis, multiple sclerosis, pro‐thrombotic state, and diffuse coagulopathy, as well as certain autoinflammatory conditions such as Kawasaki disease in children. We have reviewed the association between COVID‐19 and autoimmune disorders in this article.

Background Epstein-Barr Virus (EBV) is a human oncogenic virus that can lead to cancer in lymphoid and epithelial cells and is one of the hypothesized causes of oral cavity lesions including oral squamous cell carcinoma (OSCC), but the etiological association remains undetermined. The present investigation aimed to explore the EBV presence, viral load, and EBV-encoded small RNA (EBER) sequence variation in tissue samples of patients with OSCC and other oral cavity lesions including oral lichen planus (OLP), and oral irritation fibroma (OIF). Methods In total, 88 oral cavity samples (23 with OSCC, 29 with OLP, and 36 with OIF diagnosis) were examined by Real-Time PCR technique and some of them were sequenced. Results Viral EBER sequence was detected in 6 out of the 23 OSCC (31.4%), 6 out of the 29 OLP (20.7%), and 3 out of the 36 OIF cases (8.3%). The mean EBV copy number was higher in OSCC samples (1.2 × 10−2 ± 1.3 × 10−2 copies/cell) compared to OLP (2.2 × 10−3 ± 2.6 × 10−3 copies/cell) and OIF (2.4 × 10−4 ± 2.0 × 10−4 copies/cell) samples, although this difference was not statistically significant (P = 0.318). The EBER gene was amplified and sequenced in 5 OSCC, 3 OLP, and 2 OIF samples with high EBV viral load. One OSCC, two OLP, and two OIF isolates showed different nucleotide variations compared with EBV-WT and AG876 prototype sequences: C6834T, C6870T, C6981T, C7085T, C7085G, and C7094T. Conclusion In our study the presence of more than one genome copies per tumor cell indicates the possible role of EBV infection in oral cancers. However, more studies should be conducted to clarify the role of EBV in OSCC carcinogenesis.

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