The role of Staphylococcus aureus in cystic fibrosis pathogenesis and clinico-microbiological interactions.

Cystic fibrosis (CF) is a progressive and inherited disease that affects approximately 70000 individuals all over the world annually. A mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene serves as its defining feature. Bacterial infections have a significant impact on the occurrence and development of CF. In this manuscript, we discuss the role and virulence factors of Staphylococcus aureus as an important human pathogen with the ability to induce respiratory tract infections. Recent studies have reported S. aureus as the first isolated bacteria in CF patients. Methicillin-resistant Staphylococcus aureus (MRSA) pathogens are approximately resistant to all ß-lactams. CF patients are colonized by MRSA expressing various virulence factors including toxins, and Staphylococcal Cassette Chromosome mec (SCCmec) types, and have the potential for biofilm formation. Therefore, variations in clinical outcomes will be manifested. SCCmec type II has been reported in CF patients more than in other SCCmec types from different countries. The small-colony variants (SCVs) as specific morphologic subtypes of S. aureus with slow growth and unusual properties can also contribute to persistent and difficult-to-treat infections in CF patients. The pathophysiology of SCVs is complicated and not fully understood. Patients with cystic fibrosis should be aware of the intrinsic risk factors for complex S. aureus infections, including recurring infections, physiological issues, or coinfection with P. aeruginosa.

Epidemiological characterization of clinical isolates of meticillin resistant Staphylococcus aureus through multilocus sequence typing and staphylococcal cassette chromosome mec typing in Northwest Iran.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA), is considered a potential and aggressive nosocomial pathogen. It accounts for 50% of S. aureus isolates in tertiary hospitals in Iran, however, there is no sufficient evolutionary and epidemiological investigation about this medically important bacterium. We aimed to study the lineage and evolution of MRSA in Northwest Iran during 2021-2022 based on the obtained phenotypic and genotypic characteristics. MATERIALS AND METHODS: Seventy-two non-duplicate MRSA isolates were collected from 3 referral hospitals in Tabriz, Ardebil, and Urmia cities. The antimicrobial susceptibility patterns were determined by disk diffusion test and micro broth dilution methods. Thereafter 4 virulence genes (eta, etb, pvl, tst) and 5 types of staphylococcal cassette chromosome mec (SCCmec) were detected by PCR. In the final step, representative isolates were selected to be studied by Multilocus sequence typing (MLST). RESULTS: The highest resistance was observed to erythromycin and clindamycin at a rate of 76.4%, followed by ciprofloxacin (61.1%), gentamicin (54.2%), rifampin (38.9%), and co-trimoxazole (27.8%). All isolates were susceptible to vancomycin. The virulence genes of etb, pvl, tst, and eta were detected in 50%, 29.2%, 21.8%, and 13.9% of isolates, respectively. SCCmec types III and I were the most prevalent types, followed by types IV, II, and V. MLST analysis revealed 6 sequence types: ST6854, ST5282, ST127, ST7804, ST1607, and ST7784. Two MLST-based clonal complexes (CC8, and CC97) were identified as well. CONCLUSION: The ST numbers were non-repetitive. CC8 as a pandemic clone and an individual lineage and clinically significant clade was reported as the most prevalent clonal complex. It is essential periodic evaluations of antibiotic susceptibility patterns and study the evolutionary characteristics of medical-challenging microorganisms in particular MRSA to effectively treat and restrict the outbreaks.

SARS-CoV-2-associated organs failure and inflammation: a focus on the role of cellular and viral microRNAs.

SARS-CoV-2 has been responsible for the recent pandemic all over the world, which has caused many complications. One of the hallmarks of SARS-CoV-2 infection is an induced immune dysregulation, in some cases resulting in cytokine storm syndrome, acute respiratory distress syndrome and many organs such as lungs, brain, and heart that are affected during the SARS-CoV-2 infection. Several physiological parameters are altered as a result of infection and cytokine storm. Among them, microRNAs (miRNAs) might reflect this poor condition since they play a significant role in immune cellular performance including inflammatory responses. Both host and viral-encoded miRNAs are crucial for the successful infection of SARS-CoV-2. For instance, dysregulation of miRNAs that modulate multiple genes expressed in COVID-19 patients with comorbidities (e.g., type 2 diabetes, and cerebrovascular disorders) could affect the severity of the disease. Therefore, altered expression levels of circulating miRNAs might be helpful to diagnose this illness and forecast whether a COVID-19 patient could develop a severe state of the disease. Moreover, a number of miRNAs could inhibit the expression of proteins, such as ACE2, TMPRSS2, spike, and Nsp12, involved in the life cycle of SARS-CoV-2. Accordingly, miRNAs represent potential biomarkers and therapeutic targets for this devastating viral disease. In the current study, we investigated modifications in miRNA expression and their influence on COVID-19 disease recovery, which may be employed as a therapy strategy to minimize COVID-19-related disorders.

Dynamic alterations in white blood cell counts and SARS-CoV-2 shedding in saliva: an infection predictor parameter.

Introduction: The recent coronavirus (COVID-19) outbreak posed a global threat and quickly escalated to a pandemic. However, accurate information on potential relationships between SARS-CoV-2 shedding in body fluids, especially saliva, and white blood cell (WBC) count is limited. In the present study we investigated the potential correlation between alterations in blood cell counts and viral shedding in saliva in a cohort of COVID-19 patients. Method: In this preliminary clinical research, 24 age-matched COVID-19 patients without comorbidities, 12 (50%) men and 12 (50%) women, were followed up for a period of 5 days to investigate whether changes in the level of viral shedding in saliva might parallel with temporal alterations in WBC count. Viral shedding in saliva was qualitatively measured by performing SARS-CoV-2 rapid antigen tests on patient saliva samples, using SARS-CoV-2 Rapid Antigen Test Kit (Roche, Basel, Switzerland). These patients were classified into two groups with sputum and non-sputum cough. WBCs counts including leukocyte (LYM), neutrophil (NEU), and LYM counts were recorded for each patient on days 1, 3, and 5. Results: The results of the present study showed that the levels of WBC, LYM, and NEU as well as erythrocyte sedimentation rate (ESR) increased significantly on the 5th day compared to the first day in both groups with sputum. However, the levels of C-reactive protein (CRP), Neutrophil-to-Lymphocyte Ratio (NLR) and lactate dehydrogenase (LDH) did not show significant changes. Conclusion: This study proves that investigating the change in the number of blood LYMs as well as laboratory parameters such as CRP, LDH, and ESR as biomarkers is an accurate indicator to detect the amount of viral shedding in people with sputum and non-sputum. The results of our study denote that the measured parameters exhibit the intensity of viral shedding in people with sputum.

Interleukin-2 and Oncolytic Virotherapy: A New Perspective in Cancer Therapy.

By triggering immune responses in malignancies that have generally been linked to poor outcomes, immunotherapy has recently shown effectiveness. On the other hand, tumors provide an environment for cells that influence the body's immunity against cancer. Malignant cells also express large amounts of soluble or membrane-bound ligands and immunosuppressive receptors. In this regard, the combination of oncolytic viruses with pro-inflammatory or inflammatory cytokines, including IL-2, can be a potential therapy for some malignancies. Indeed, oncolytic viruses cause the death of cancerous cells and destroy the tumor microenvironment. They result in the local release of threat signals and antigens associated with tumors. As a result, it causes lymphocyte activity and the accumulation of antigenpresenting cells which causes them to accumulate in the tumor environment and release cytokines and chemokines. In this study, we reviewed the functions of IL-2 as a crucial type of inflammatory cytokine in triggering immune responses, as well as the effect of its release and increased expression following combination therapy with oncolytic viruses in the process of malignant progression, as an essential therapeutic approach that should be taken into consideration going forward.

Immune-checkpoint expression in antigen-presenting cells (APCs) of cytomegaloviruses infection after transplantation: as a diagnostic biomarker.

Cytomegalovirus (CMV), a member of the Herpesviridae family, mostly causes only slight feverish symptoms or can be asymptomatic in immunocompetent individuals. However, it is known to be particularly a significant cause of morbidity in immunocompromised patients, including transplant recipients, whose immune system has been weakened due to the consumption of immunosuppressor drugs. Therefore, the diagnosis of CMV infection after transplantation is crucial. New diagnostic methods for the quick detection of CMV have been developed as a result of understanding the clinical importance of invasive CMV. Antigen-presenting cells (APCs) and T cells are important components of the immune system and it may be possible to diagnose viral infections using immunological markers, such as lymphocytosis, cytotoxic T lymphocytes (CTL), and serum cytokine levels. Moreover, PD-1, CTLA 4, and TIGIT, which are expressed on certain T cells and antigen-presenting cells, are over-expressed during the infection. The assessment of CMV infection based on T cell and APC activity, and the expression of immunological checkpoints, can be helpful for the diagnosis of transplant patients at risk for CMV infection. In this review, we will investigate how immune checkpoints affect immune cells and how they impair organ transplantation after CMV infection.

PBMC MicroRNAs: Promising Biomarkers for the Differential Diagnosis of COVID-19 Patients with Abnormal Coagulation Indices.

MicroRNAs, or miRNAs, may involve in coagulation and inflammation pathways caused by severe Coronavirus disease (COVID-19). Accordingly, this attempt was made to explore the behavior of peripheral blood mononuclear cells (PBMCs) miRNAs as effective biomarkers to diagnose COVID-19 patients with normal and abnormal coagulation indices. We selected the targeted miRNAs (miR-19a-3p, miR-223-3p, miR-143-5p, miR-494-3p and miR-301a-5p) according to previous reports, whose PBMC levels were then determined by real-time PCR. Receiver operating characteristic (ROC) curve was obtained to clarify the diagnostic potency of studied miRNAs. The differentially expressed miRNA profiles and corresponding biological activities were predicted in accordance with bioinformatics data. Targeted miRNAs' expression profiles displayed a significant difference between COVID-19 subjects with normal and abnormal coagulation indices. Moreover, the average miR-223-3p level expressed in COVID-19 cases with normal coagulation indices was significantly lower than that in healthy controls. Based on data from ROC analysis, miR-223-3p and miR-494-3p are promising biomarkers to distinguish the COVID-19 cases with normal or abnormal coagulation indices. Bioinformatics data highlighted the prominent role of selected miRNAs in the inflammation and TGF-beta signaling pathway. The differences existed in the expression profiles of selected miRNAs between the groups introduced miR-494-3p and miR-223-3p as potent biomarkers to prognosis the incidence of COVID-19.

A comprehensive review of COVID-19 symptoms and treatments in the setting of autoimmune diseases.

After the first reporting of the index case of Severe Acute Respiratory Syndrome (SARS)-CoV-2-associated disease at the end of December 2019, the virus spread quickly throughout the world, prompting the WHO on 11 March 2020 to declare the disease a global pandemic. The coronavirus disease 2019 (COVID-19) pandemic, raises concerns for all people, mainly for susceptible population. People with pre-existing diseases, especially individuals with autoimmune disorders, are more at the risk of SARS-CoV-2 infection because of compromised immune system due to frequent use of immunosuppressive drugs and steroids. Patients with autoimmune diseases and their physicians have concerns about these patients' healthcare, since they are at a higher risk for COVID-19 infection, may show severe complications of COVID-19, and may experience probable flares of their pre-existing disease. Even though there have been several studies discussing the relation between COVID-19 and various types of autoimmune diseases, it cannot be ascertained that all patients with autoimmune diseases experience more severe complications of COVID-19 and have more hospitalization or mortality rate. The situation depends on each patient's condition, such as the type and the severity of the underlying autoimmune disease and the kind of treatment they receive. In the present review, we have discussed the effects of COVID-19 pandemic on patients with different autoimmune diseases and their relative concerns about their treatments. As a result, we have reviewed further considerations that should be taken into account for these patients during the pandemic or when they are infected with COVID-19.

Monoclonal antibodies in cervical malignancy-related HPV.

Despite many efforts to treat HPV infection, cervical cancer survival is still poor for several reasons, including resistance to chemotherapy and relapse. Numerous treatments such as surgery, radiation therapy, immune cell-based therapies, siRNA combined with various drugs, and immunotherapy are being studied and performed to provide the best treatment. Depending on the stage and size of the tumor, methods such as radical hysterectomy, pelvic lymphadenectomy, or chemotherapy can be utilized to treat cervical cancer. While accepted, these treatments lead to interruptions in cellular pathways and immune system homeostasis. In addition to a low survival rate, cervical neoplasm incidence has been rising significantly. However, new strategies have been proposed to increase patient survival while reducing the toxicity of chemotherapy, including targeted therapy and monoclonal antibodies. In this article, we discuss the types and potential therapeutic roles of monoclonal antibodies in cervical cancer.

The role of antigen-presenting cells in the pathogenesis of COVID-19.

Coronavirus Disease 2019 (COVID-19) is one of the three lethal coronavirus outbreaks in the recent two decades and a serious threat to global health all over the world. The principal feature of the COVID-19 infection is the so-called "cytokine storm" exaggerated molecular response to virus distribution, which plays massive tissue and organ injury roles. Immunological treatments, including monoclonal antibodies and vaccines, have been suggested as the main approaches in treating and preventing this disease. Therefore, a proper investigation of the roles of antigen-presenting cells (APCs) in the aforementioned immunological responses appears essential. The present review will provide detailed information about APCs' role in the infection and pathogenesis of SARS-CoV-2 and the effect of monoclonal antibodies in diagnosis and treatment.

SARS-CoV-2: Receptor and Co-receptor Tropism Probability.

The recent pandemic which arose from China, is caused by a pathogenic virus named "severe acute respiratory syndrome-related coronavirus-2 (SARS-CoV-2)". Its rapid global expansion has inflicted an extreme public health concern. The attachment of receptor-binding domains (RBD) of the spike proteins (S) to the host cell's membrane, with or without the help of other cellular components such as proteases and especially co-receptors, is required for the first stage of its pathogenesis. In addition to humans, angiotensin-converting enzyme 2 (ACE2) is found on a wide range of vertebrate host's cellular surface. SARS-CoV-2 has a broad spectrum of tropism; thus, it can infect a vast range of tissues, organs, and hosts; even though the surface amino acids of the spike protein conflict in the receptor-binding region. Due to the heterogeneous ACE2 distribution and the presence of different domains on the SARS-CoV-2 spike protein for binding, the virus entry into diverse host cell types may depend on the host cells' receptor presentation with or without co-receptors. This review investigates multiple current types of receptor and co-receptor tropisms, with other molecular factors alongside their respective mechanisms, which facilitate the binding and entry of SARS-CoV-2 into the cells, extending the severity of the coronavirus disease 2019 (COVID-19). Understanding the pathogenesis of COVID-19 from this perspective can effectively help prevent this disease and provide more potent treatment strategies, particularly in vulnerable people with various cellular-level susceptibilities.

The effect of Wnt/ß-catenin signaling on PD-1/PDL-1 axis in HPV-related cervical cancer.

Infection with high-risk human papillomavirus (HPV), including HPV-16 and HPV-18, is the main cause of malignancies, such as cervical cancer. Viral oncoproteins encoded by HPV are expressed in HPV-positive cancers and associated with the early cancer stages and the transformation of normal cells. The signaling pathways involved in the transformation of normal cells to cancerous form and the subsequently expressed programmed cell death-ligand 1 (PD-L1) on the surface of the transformed cells lead to a disruption in recognition of tumor cells by the immune cell system, including T lymphocytes and dendritic cells which lead to the development of cervical cancer malignancy. These cells also produce modest levels of cytokines during exhaustion, tumor-infiltrating T CD4+ cells with high levels of PD-1 and CD39 release considerable quantities of cytokines. The Wnt/ß-catenin signaling pathway, which controls the expression of genes involved in the tumor cells' markers, is demonstrated to be one of the most potent cancer stimulants. It leads to the evasion of the tumor cells from immune cell detection and ultimately avoids being recognized by dendritic cells or T-cells. PD-L1, as an inhibitory immune checkpoint, is essential for controlling immune system activity by inhibiting T-cells' inflammatory function. In the present review, we looked into how Wnt/ß-catenin affects the expression of PD-L1 and related genes like c-MYC in cancer cells and its role in the development of HPV-induced malignancy. We hypothesized that blocking these pathways could be a potential immunotherapy and cancer prevention method.

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer.

BACKGROUND: This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein-Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development. METHODS: This case-control study was conducted on 67 patients with PCa and 40 control subjects. The expression levels of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantified, using the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) assay. RESULTS: The EBV/HPV coinfection was reported in 14.9% of patients in the case group and 7.5% of the control subjects. The high-risk types of HPV, that is, HPV 16 and HPV 18, were responsible for 50 and 30% of HPV/EBV-coinfected PCa cases (n = 10), respectively. No significant relationship was observed between PCa and HPV/EBV coinfection (OR = 2.9, 95% CI: 0.18-45.2, P = 0.31). However, the highest percentage of HPV genome integration was found in the HPV/EBV-coinfected PCa group (8/10; 80%). Also, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin) were significantly higher in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Nevertheless, the tumor-suppressor proteins (p53 and pRb) and E-cadherin (inhibitor of anoikis resistance) showed significant downregulations in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. CONCLUSION: The HPV/EBV coinfection may be an etiological factor for PCa through modulation of cellular behaviors.

Chitosan-Based Nanoparticles Against Viral Infections.

Viral infections, in addition to damaging host cells, can compromise the host immune system, leading to frequent relapse or long-term persistence. Viruses have the capacity to destroy the host cell while liberating their own RNA or DNA in order to replicate within additional host cells. The viral life cycle makes it challenging to develop anti-viral drugs. Nanotechnology-based approaches have been suggested to deal effectively with viral diseases, and overcome some limitations of anti-viral drugs. Nanotechnology has enabled scientists to overcome the challenges of solubility and toxicity of anti-viral drugs, and can enhance their selectivity towards viruses and virally infected cells, while preserving healthy host cells. Chitosan is a naturally occurring polymer that has been used to construct nanoparticles (NPs), which are biocompatible, biodegradable, less toxic, easy to prepare, and can function as effective drug delivery systems (DDSs). Furthermore, chitosan is Generally Recognized as Safe (GRAS) by the US Food and Drug Administration (U.S. FDA). Chitosan NPs have been used in drug delivery by the oral, ocular, pulmonary, nasal, mucosal, buccal, or vaginal routes. They have also been studied for gene delivery, vaccine delivery, and advanced cancer therapy. Multiple lines of evidence suggest that chitosan NPs could be used as new therapeutic tools against viral infections. In this review we summarize reports concerning the therapeutic potential of chitosan NPs against various viral infections.

Acute and post-acute phase of COVID-19: Analyzing expression patterns of miRNA-29a-3p, 146a-3p, 155-5p, and let-7b-3p in PBMC.

BACKGROUND: When a new pathogen, such as severe acute respiratory syndrome coronavirus 2, appears all novel information can aid in the process of monitoring and in the diagnosis of the coronavirus disease (COVID-19). The aim of the current study is to elucidate the specific miRNA profile which can act as new biomarkers for distinguishing acute COVID-19 disease from the healthy group and those in the post-acute phase of the COVID-19 disease. METHODS: The expression level of selected miRNAs including let-7b-3p, miR-29a-3p, miR-146a-3p and miR-155-5p were evaluated in peripheral blood mononuclear cells (PBMCs) of COVID-19 patients, in both the acute and post-acute COVID-19 phase of the disease and healthy groups, by real-time PCR assays. Specificity and sensitivity of miRNAs was tested by receiver operating characteristic (ROC) analysis in COVID-19 patients. RESULTS: The expression level of all miRNAs in COVID-19 patients was significantly higher than in the healthy group. Therefore, the expression pattern of miR-29a-3p, miR-146a-3p and let-7b-3p in the post-acute COVID-19 phase was significantly different from the acute COVID-19 phase. ROC analyses demonstrated that miR-29a-3p, -155-5p and -146a-3p may serve as the novel biomarker for COVID-19 diagnosis with high specificity and sensitivity. In addition, miR-29a-3p, and -146a-3p can maybe act as novel biomarkers for distinguishing acute from post-acute phase of COVID-19 disease. DISCUSSION: The difference in miRNA expression pattern between COVID-19 patients and those in the healthy group, and between acute COVID-19 with post-acute COVID-19, suggested that cellular miRNAs could be used as promising biomarkers for diagnosis and monitoring of COVID-19.

The roles of signaling pathways in SARS-CoV-2 infection; lessons learned from SARS-CoV and MERS-CoV.

The number of descriptions of emerging viruses has grown at an unprecedented rate since the beginning of the 21st century. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), is the third highly pathogenic coronavirus that has introduced itself into the human population in the current era, after SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV). Molecular and cellular studies of the pathogenesis of this novel coronavirus are still in the early stages of research; however, based on similarities of SARS-CoV-2 to other coronaviruses, it can be hypothesized that the NF-κB, cytokine regulation, ERK, and TNF-α signaling pathways are the likely causes of inflammation at the onset of COVID-19. Several drugs have been prescribed and used to alleviate the adverse effects of these inflammatory cellular signaling pathways, and these might be beneficial for developing novel therapeutic modalities against COVID-19. In this review, we briefly summarize alterations of cellular signaling pathways that are associated with coronavirus infection, particularly SARS-CoV and MERS-CoV, and tabulate the therapeutic agents that are currently approved for treating other human diseases.

SARS-CoV-2 infection: The role of PD-1/PD-L1 and CTLA-4 axis.

The outbreak of SARS-CoV-2 in Wuhan of China in December 2019 and its worldwide spread has turned into the COVID-19 pandemic. Respiratory disorders, lymphopenia, cytokine cascades, and the immune responses provoked by this virus play a major and fundamental role in the severity of the symptoms and the immunogenicity which it causes. Owing to the decrease in the inflammatory responses' regulation in the immune system and the sudden increase in the secretion of cytokines, it seems that an investigation of inhibitory immune checkpoints can influence theories regarding this disease's treatment methods. Acquired cell-mediated immune defense's T-cells have a key major contribution in clearing viral infections thus reducing the severity of COVID-19's symptoms. The most important diagnostic feature in individuals with COVID-19 is lymphocyte depletion, most importantly, T-cells. Due to the induction of interferon-γ (INF-γ) production by neutrophils and monocytes, which are abundantly present in the peripheral blood of the individuals with COVID-19, the expression of inhibitory immune checkpoints including, PD-1 (programmed death), PD-L1 and CTLA4 on the T-cells' surface is enhanced. The purpose of this review is to discuss the functions of these checkpoints and their effects on the dysfunction and exhaustion of T-cells, making them almost ineffective in individuals with COVID-19, especially in the cases with extreme symptoms.

Tightly controlled response to oxidative stress; an important factor in the tolerance of Bacteroides fragilis.

The exposure of Bacteroides fragilis to highly oxygenated tissues induces an oxidative stress due to a shift from the reduced condition of the gastrointestinal tract to an aerobic environment of host tissues. The potent and effective responses to reactive oxygen species (ROS) make the B. fragilis tolerant to atmospheric oxygen for several days. The response to oxidative stress in B. fragilis is a complicated event that is induced and regulated by different agents. In this review, we will focus on the B. fragilis response to oxidative stress and present an overview of the regulators of responses to oxidative stress in this bacterium.

The role of Th17 cells in viral infections.

The present review provides an overview of recent advances regarding the function of Th17 cells and their produced cytokines in the progression of viral diseases. Viral infections alone do not lead to virus-induced malignancies, as both genetic and host safety factors are also involved in the occurrence of malignancies. Acquired immune responses, through the differentiation of Th17 cells, form the novel components of the Th17 cell pathway when reacting with viral infections all the way from the beginning to its final stages. As a result, instead of inducing the right immune responses, these events lead to the suppression of the immune system. In fact, the responses from Th17 cells during persistent viral infections causes chronic inflammation through the production of IL-17 and other cytokines which provide a favorable environment for tumor growth and its development. Additionally, during the past decade, these cells have been understood to be involved in tumor progression and metastasis. However, further research is required to understand Th17 cells' immune mechanisms in the vast variety of viral diseases. This review aims to determine the roles and effects of the immune system, especially Th17 cells, in the progression of viral diseases; which can be highly beneficial for the diagnosis and treatment of these infections.