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Human monkeypox virus (MPXV) is a double-stranded DNA virus of the Orthopoxvirus genus of the Poxviridae family. Two genetic clades of the monkeypox virus have been identified: West African and Central African.

Coronaviruses were first discovered in the 1960s and are named due to their crown-like shape. Sometimes, but not often, a coronavirus can infect both animals and humans. An acute respiratory disease, caused by a novel coronavirus (severe acute respiratory syndrome coronavirus-2 or SARS-CoV-2 previously known as 2019-nCoV) was identified as the cause of coronavirus disease 2019 (COVID-19) as it spread throughout China and subsequently across the globe. As of 14th July 2020, a total of 13.1 million confirmed cases globally and 572,426 deaths had been reported by the World Health Organization (WHO). SARS-CoV-2 belongs to the β-coronavirus family and shares extensive genomic identity with bat coronavirus suggesting that bats are the natural host. SARS-CoV-2 uses the same receptor, angiotensin-converting enzyme 2 (ACE2), as that for SARS-CoV, the coronavirus associated with the SARS outbreak in 2003. It mainly spreads through the respiratory tract with lymphopenia and cytokine storms occuring in the blood of subjects with severe disease. This suggests the existence of immunological dysregulation as an accompanying event during severe illness caused by this virus. The early recognition of this immunological phenotype could assist prompt recognition of patients who will progress to severe disease. Here we review the data of the immune response during COVID-19 infection. The current review summarizes our understanding of how immune dysregulation and altered cytokine networks contribute to the pathophysiology of COVID-19 patients.

The life span of patients with primary and secondary immunodeficiency is increasing due to recent improvements in therapeutic strategies. While the incidence of primary immunodeficiencies (PIDs) is 1:10,000 births, that of secondary immunodeficiencies are more common and are associated with posttransplantation immune dysfunction, with immunosuppressive medication for human immunodeficiency virus or with human T-cell lymphotropic virus infection. After infection, malignancy is the most prevalent cause of death in both children and adults with (PIDs). PIDs more often associated with cancer include common variable immunodeficiency (CVID), Wiskott-Aldrich syndrome, ataxia-telangiectasia, and severe combined immunodeficiency. This suggests that a protective immune response against both infectious non-self-(pathogens) and malignant self-challenges (cancer) exists. The increased incidence of cancer has been attributed to defective elimination of altered or \"transformed\" cells and/or defective immunity towards cancer cells. The concept of aberrant immune surveillance occurring in PIDs is supported by evidence in mice and from patients undergoing immunosuppression after transplantation. Here, we discuss the importance of PID defects in the development of malignancies and the current limitations associated with molecular pathogenesis of these diseases and emphasize the need for further knowledge of how specific mutations can modulate the immune system to alter immunosurveillance and thereby play a key role in the etiology of malignancies in PID patients.

Patients with tuberculous pleural effusion (TPE) or malignant pleural effusions (MPE) frequently have similar pleural fluid profiles. New biomarkers for the differential diagnosis of TPE are required. We determined whether cytokine profiles in the PE of patients could aid the differential diagnosis of TPE. 30 patients with TPE, 30 patients with MPE, 14 patients with empyema (EMP) and 14 patients with parapneumonic effusion (PPE) were enrolled between Dec 2018 and 2019. The levels of interleukin (IL)-6, IL-18, IL-27, CXCL8, CCL-1 and IP-10 were determined in PE by ELISA along with measurements of adenosine deaminase (ADA). The best predictors of TPE were combined ADA.IL-27 [optimal cut-off value = 42.68 (10 3  U ng/l 2 ), sensitivity 100%, specificity 98.28%], ADA [cut off value 27.5 (IU/l), sensitivity 90%, specificity 96.5%] and IL-27 [cut-off value = 2363 (pg/ml), sensitivity 96.7%, specificity 98.3%, p ≤ 0.0001]. A high level of IL-6 [cut-off value = 3260 (pg/ml), sensitivity 100%, specificity 67.2%], CXCL8 [cut-off value = 144.5 (pg/ml), sensitivity 93.3%, specificity 58.6%], CCL1 [cut-off value = 54 (pg/ml), sensitivity 100%, specificity 70.7%] and IP-10 [cut-off value = 891.9 (pg/ml), sensitivity 83.3%, specificity 48.3%] were also predictive of TPE. High ADA.IL-27, ADA and IL-27 levels differentiate between TPE and non-TPE with improved specificity and diagnostic accuracy and may be useful clinically.

Background Influenza-associated invasive pulmonary aspergillosis (IPA) is a known complication of influenza in the intensive care unit (ICU) but limited information is evident for non-ICU patients. Methods In this cross-sectional study, we retrospectively collected electronic medical records of all patients admitted to the medical infectious disease ward who had confirmed influenza and met the criteria for invasive aspergillosis. This study recruited patients between September 2023 to May 2024 from the Masih Daneshvari Educational Pulmonary Referral Center in Iran. Results Among 109 patients with confirmed influenza, 10 were diagnosed with IPA. Our findings indicated that the odds of death were significantly higher in patients with IPA compared to those without it (Odds Ratio [OR] = 20.78, 95% Confidence Interval [CI] [2.97 to 145.61], P  = 0.005). The rate of bacterial co-infections was also elevated in patients with IPA compared to those without (OR = 4.7, 95% CI [1.22 to 18.01], P  = 0.025). Patients with IPA had a greater likelihood of being transferred to the ICU (OR = 3.4, 95% CI [0.77 to 15.2], P  = 0.118). They experienced longer hospital stays, with a median duration of 19.5 days (Interquartile Range [IQR] [11.7–26.5]) compared to 7 days (IQR [6–12]) for those without IPA (Z = -3.8, P  < 0.001). Furthermore, patients with IPA had a significantly higher likelihood of having underlying lung disease compared to their counterparts without IPA (OR = 67, 95% CI [1.3 to 33.3], P  = 0.015). Conclusions This study found that IPA is a lethal complication of influenza among non-ICU patients with Influenza.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has infected over 112M patients and resulted in almost 2.5M deaths worldwide. The major clinical feature of severe COVID-19 patients requiring ventilation is acute respiratory distress syndrome (ARDS) possibly associated with a cytokine storm. To elucidate serum levels of TNF-α and soluble TNF-Receptor 1 (sTNFR1) in patients with severe and mild COVID-19 disease as determinants of disease severity. We determined serum TNF-α and sTNFR1 concentrations in 46 patients with laboratory-confirmed COVID-19 (17 patients with severe disease within the intensive care unit [ICU] and 29 non-severe, non-ICU patients) and 15 healthy controls upon admission using ELISA. Subjects were recruited between March-May 2020 at the Masih Daneshvari Hospital Tehran, Iran. Serum levels of sTNFRI were significantly higher in ICU patients (P<0.0001) and non-ICU patients (P=0.0342) compared with healthy subjects. Serum sTNFR1 were significantly higher in ICU patients than in non-ICU patients (P<0.0001). Serum TNF-α levels were greater in ICU and non-ICU patients than in the healthy subjects group (p<0.0001). The sTNFRI concentration in ICU (r=0.79, p=0.0002) and non-ICU (r=0.42, p=0.02) patients positively correlated with age although serum sTNFRI levels in ICU patients were significantly higher than in older healthy subjects. The sTNFRI concentration in ICU patients negatively correlated with ESR. The study demonstrates higher sTNFRI in ICU patients with severe COVID-19 disease and this be a biomarker of disease severity and mortality. Future studies should examine whether lower levels of systemic sTNFR1 at admission may indicate a better disease outcome.

Background and objectives Migration, as an important social determinant in the field of health, plays a crucial role in the non-eradication of tuberculosis worldwide. Therefore, it is essential to identify the factors related to tuberculosis treatment in immigrants to effectively combat this disease. However no comprehensive study has focused on this issue. Therefore, this study was conducted using an ecological approach to identify the barriers and facilitators of tuberculosis treatment in immigrants. Methods This qualitative study utilized an integrative literature review. Studies were searched without time restrictions in database such as MEDLINE, Institute for Scientific Information (ISI), Google Scholar, Scopus, and EMBAS, as well as internal databases like Scientific Information Database and Magiran. The findings of 100 studies that met the inclusion criteria were analyzed using the conventional content analysis method based on the ecological approach. Results In general, the aforementioned codes were placed into four main categories, including individual factors (i.e., biological factors, psychological factors, behavioral factors, patient knowledge, factors related to tuberculosis, and economic factors), interpersonal factors (i.e., communication with the treatment team and family-related factors), factors related to health service provider centers (i.e., medical facilities), and extra-organizational factors (i.e., social factors and health policies). Conclusion The findings of the present study show that treating tuberculosis in immigrants is a complex phenomenon influenced by several factors. Therefore policymakers and healthcare providers should take a more comprehensive look at the factors affecting treatment in this group of patients to plan and implement more effective interventions.

ISG15 is an interferon (IFN)-α/β-induced ubiquitin-like protein. It exists as a free molecule, intracellularly and extracellularly, and conjugated to target proteins. Studies in mice have demonstrated a role for Isg15 in antiviral immunity. By contrast, human ISG15 was shown to have critical immune functions, but not in antiviral immunity. Namely, free extracellular ISG15 is crucial in IFN-γ-dependent antimycobacterial immunity, while free intracellular ISG15 is crucial for USP18-mediated downregulation of IFN-α/β signalling. Here we describe ISG15 -deficient patients who display no enhanced susceptibility to viruses in vivo , in stark contrast to Isg15 -deficient mice. Furthermore, fibroblasts derived from ISG15 -deficient patients display enhanced antiviral protection, and expression of ISG15 attenuates viral resistance to WT control levels. The species-specific gain-of-function in antiviral immunity observed in ISG15 deficiency is explained by the requirement of ISG15 to sustain USP18 levels in humans, a mechanism not operating in mice. ISG15 is a ubiquitin-like protein which has important immune-related functions in mice and humans. Here the authors demonstrate that, unlike in mice, human ISG15 stabilizes UPS18 and that ISG15-deficient human cells are more resistant to viral infection.

Human herpesvirus 8 (HHV‐8), also known as Kaposi sarcoma‐associated herpesvirus (KSHV), causes multiple cancers, particularly Kaposi sarcoma (KS), which continues to be a major health concern for patients with severe HIV/AIDS. When KS affects the lungs, it can create diagnostic difficulties, especially when it appears as chest fluid accumulation without characteristic lesions. We describe an unusual case involving a 27‐year‐old HIV‐positive female patient with skin KS who developed worsening breathing problems and was discovered to have hemorrhagic pleural effusion. Medical imaging showed bilateral massive pleural effusions with adjacent compressive atelectasis. HHV‐8 genetic material was identified in the pleural effusion, and surgical examination revealed small nodular growths on the visceral and parietal pleural surfaces; nevertheless, microscopic tissue analysis indicated a reactive, non‐cancerous chest lining response. Other infectious and tumor‐related causes were eliminated. Treatment with antiretroviral medications and encapsulated doxorubicin resulted in marked clinical improvement. This case highlights the necessity of including widespread KS as a diagnostic possibility in HIV‐positive patients presenting with hemorrhagic pleural effusion. Identifying HHV‐8 in chest fluid combined with typical clinical characteristics can support the diagnosis. Early treatment with antiretroviral therapy and cancer medications can produce significant clinical improvement.

The coronavirus disease of 2019 (COVID-19) resulted from an infection by severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) which is the main cause of acute respiratory distress syndrome (ARDS) in global population from 2019 on. It may contribute to higher rate of death among the patients with immunodeficiency based on recent reports. In addition, Good syndrome (GS) as a result of thymoma removal might cause in some long-lasting microbial infections. We described clinical aspects and viral mutations on a case of GS suffering from COVID-19. A 46-year-old man with fever, common respiratory disease symptoms and positive COVID-19 polymerase chain reaction (PCR) test, with the history of thymoma removal surgery was admitted to Masih Daneshvari Hospital, Tehran, Iran. Lung radiographs and oxygen saturation measurement disclosed considerable implication resulted in application of several anti-microbial medication. The delta variant (B.1.617.2 (21 J Clade)) was the strain isolated from the patient by sequencing methods done by the COVID-19 National Reference Laboratory (CNRL), Pasteur Institute of Iran, while the dominant strain circulated mostly among population was Omicron (B.1.1.529) at the time of sampling. Unfortunately, the patient had passed away a month later by sudden respiratory failure progressed in refractory septic shock. Despite the fact that opportunistic infections may lead the GS patients to a major health problematic condition, unusual persistent of infections such as non-dominant variant of SARS-Cov-2 could be observed through the disease timeline. Therefore, a fully screening of thymoma plus intra-host evolution monitoring of SARS-CoV-2 is highly recommended in immunocompromised patients.