Interleukin-35 (IL-35), is a recently identified cytokine that belongs to the IL-12 family, it is a potent antiinflammatory and immunosuppressive cytokine which was first recognized to be produced by regulatory T cells (Tregs) cells, and recently was found to be produced by regulatory B cells (Bregs). The study aimed at determining whether plasma levels of IL-35 are associated with clinical characteristics of breast cancer (BC) patients. The study included 40 patients with breast cancer (BC), and 10 matched controls. The IL-35 cytokine was measured in plasma using ELISA. Results showed that plasma IL-35levels were significantly higher in BC than healthy controls (P˂ 0.05), and were significantly associated with BC grade 2 and HER-2 over expression level “3+”, suggesting that plasma IL-35 levels may be associated with the development and progression of BC.

Stenotrophomonas maltophilia is an opportunistic multidrug resistant pathogen causing hospital-acquired infections (HAIs) with limited treatment options. We aimed to determine the prevalence of S. maltophila causing HAIs and environmental contamination in the intensive care units (ICUs) and wards of Assiut University Hospitals. We determined the antibiotic resistance profiles of, production of metallo-β-lactamases (MBLs) by, and the presence of the sul II gene in these isolates. The study included 362 patients with HAIs and 4151 environmental samples from the ICUs and wards. Antibiotic sensitivities were tested by the disc diffusion method; imipenem minimum inhibitory concentration (MIC) was determined using the E-test. Metallo-β-lactamase enzymes (MBLs) were detected phenotypically by combined disc test (CDT) and double disc synergy test (DDST). The sul ΙΙ gene was detected by polymerase chain reaction. The percentages of S. maltophilia causing infections and environmental contamination were found to be 9.7% and 0.67% respectively. Respiratory tract infection was the most common infection (17.97%). Isolates were highly resistant to aztreonam, penicillins, carbapenems, quinolones, cephalosporins, aminoglycosides, chloramphenicol and tetracyclines, and least resistant to trimethoprim- sulfamethoxazole (SXT). All imipenem resistant isolates (82.54%) showed MBL phenotypically by both tests. For imipenem sensitive isolates (17.46%), MBL was detected by DDST and CDT in 36.36% and 18.18% respectively. Isolates resistant to SXT had sul II genes. In conclusion, S. maltophilia is a significant hospital pathogen at Assiut University Hospitals with high percentages of resistance to many antimicrobials, making the possibility of dissemination worrisome. In our setting, SXT is the agent of choice for the treatment of S. maltophilia infections

Viruses can trigger glomerulonephritis (GN) development. Hepatitis viruses, especially Hepatitis C virus and Hepatitis B viruses, are examples of the viruses that trigger GN initiation or progression. However, the proof of a correlation between GN and Hepatitis E virus infection is not clear. Some studies confirmed the development of GN during acute or chronic HEV infections, mainly caused by genotype 3. While others reported that there is no relation between HEV exposure and GN development. A recent study showed that a reduced glomerular filtration rate was developed in 16% of acute HEV genotype 1 (HEV-1) infections that returned to normal during recovery. HEV-1 is endemic in Egypt with a high seroprevalence among villagers and pregnant women. There is no available data about a link between HEV and GN in Egypt. Methods: GN patients (n = 43) and matched healthy subjects (n = 36) enrolled in Assiut University hospitals were included in this study. Blood samples were screened for hepatotropic pathogens. Tests for HEV markers such as HEV RNA and anti-HEV antibodies (IgM and IgG) were performed. Laboratory parameters were compared in HEV-seropositive and HEV-seronegative GN patients. Results: Anti-HEV IgG was detected in 26 (60.5%) out of 43 GN patients. HEV seroprevalence was significantly higher in GN than in healthy controls, suggesting that HEV exposure is a risk factor for GN development. None of the GN patients nor the healthy subjects were positive for anti-HEV IgM or HEV RNA. There was no significant difference between seropositive and seronegative GN patients in terms of age, gender, albumin, kidney function profiles, or liver transaminases. However, anti-HEV IgG positive GN patients had higher bilirubin levels than anti-HEV IgG negative GN patients. HEV-seropositive GN patients had a significantly elevated AST level compared to HEV-seropositive healthy subjects. Conclusion: exposure to HEV infection could be complicated by the development of GN.

Hepatitis A virus (HAV) and Hepatitis E virus (HEV) are transmitted through the fecal–oral route. HAV outbreaks and one HEV outbreak have been reported in Egypt. However, the impact of HAV–HEV co-infection is not known. In this study, we assessed HEV markers in acute HAV-infected patients (n = 57) enrolled in Assiut University hospitals. We found that 36.8% of HAV-infected patients were also positive for HEV markers (anti-HEV IgM and HEV RNA), while 63.2% of the patients were HAV mono-infected. Demographic and clinical criteria were comparable in both HAV mono-infected patients and HAV–HEV co-infected patients. Although liver enzymes were not significantly different between the two groups, liver transaminases were higher in the co-infected patients. Six patients developed acute liver failure (ALF); five of them were HAV–HEV-co-infected patients. The relative risk of ALF development was 8.5 times higher in HAV–HEV co-infection compared to mono-infection. Three cases of ALF caused by HAV–HEV co-infection were reported in children (below 18 years) and two cases were reported in adults. All patients developed jaundice, coagulopathy, and encephalopathy; all were living in rural communities. In conclusion: HAV–HEV co-infection can be complicated by ALF. The risk of ALF development in HAV-infected patients is higher when coinfection with HEV is present.

Viral infections trigger inflammation by controlling ATP release. CD39 ectoenzymes hy drolyze ATP/ADP to AMP, which is converted by CD73 into anti-inflammatory adenosine (ADO). ADOisananti-inflammatory and immunosuppressant molecule which can enhance viral persistence and severity. The CD39-CD73-adenosine axis contributes to the immunosuppressive T-reg microenvi ronment and mayaffect COVID-19 disease progression. Here, we investigated the link between CD39 expression, mostly on T-regs, and levels of CD73, adenosine, and adenosine receptors with COVID-19 severity and progression. Our study included 73 hospitalized COVID-19 patients, of which 33 were moderately affected and 40 suffered from severe infection. A flow cytometric analysis was used to analyze the frequency of T-regulatory cells (T-regs), CD39+ T-regs, and CD39+CD4+ T-cells. Plasma concentrations of adenosine, IL-10, and TGF-β were quantified via an ELISA. An RT-qPCR was used to analyze the gene expression of CD73 and adenosine receptors (A1, A2A, A2B, and A3). T-reg cells were higher in COVID-19 patients compared to healthy controls (7.4 ± 0.79 vs. 2.4 ± 0.28; p <0.0001). Patients also had a higher frequency of the CD39+ T-reg subset. In addition, patients whosuffered from a severe form of the disease had higher CD39+ T-regs compared with moderately infected patients. CD39+CD4+ T cells were increased in patients compared to the control group. An analysis of serum adenosine levels showed a marked decrease in their levels in patients, particularly those suffering from severe illness. However, this was paralleled with a marked decline in the expression levels of CD73. IL-10 and TGF-β levels were higher in COVID-19; in addition, their values were also higher in the severe group. In conclusion, there are distinct immunological alterations in CD39+lymphocyte subsets and a dysregulation in the adenosine signaling pathway in COVID-19 patients which may contribute to immune dysfunction and disease progression. Understanding these immunological alterations in the different immune cell subsets and adenosine signaling provides valuable insights into the pathogenesis of the disease and may contribute to the development of novel therapeutic approaches targeting specific immune mechanisms

CD39 is a marker of immune cells such as lymphocytes and monocytes. The CD39/CD73 pathway hydrolyzes ATP into adenosine, which has a potent immunosuppressive effect. CD39 regulates the function of a variety of immunologic cells through the purinergic signaling pathways. CD39+Tcells have been implicated in viral infections, including Human Immunodeficiency Virus (HIV), Cytomegalovirus (CMV), viral hepatitis, and Corona Virus Disease 2019 (COVID-19) infec tions. The expression of CD39 is an indicator of lymphocyte exhaustion, which develops during chronicity. During RNA viral infections, the CD39 marker can profile the populations of CD4+ T lymphocytes into two populations, T-effector lymphocytes, and T-regulatory lymphocytes, where CD39 is predominantly expressed on the T-regulatory cells. The level of CD39 in T lymphocytes can predict the disease progression, antiviral immune responses, and the response to antiviral drugs. Besides, the percentage of CD39 and CD73 in B lymphocytes and monocytes can affect the status of viral infections. In this review, we investigate the impact of CD39 and CD39-expressing cells on viral infections and how the frequency and percentage of CD39+ immunologic cells determine disease prognosis.