This study aimed to assess the humoral immune response following administration of a BNT162b2 mRNA COVID-19 booster dose and to evaluate its association with the development of SARS-CoV-2 infection after vaccination. Between July 2021 and February 2022, serum samples were collected from 313 individuals 28 days after receiving a COVID-19 booster dose. Quantitative SARS-CoV-2 IgG antibodies directed against the receptor-binding domain (RBD) of the spike protein were measured using a chemiluminescent microparticle immunoassay. Neutralizing antibody activity, defined as inhibition of the RBD-ACE2 interaction, was evaluated semi-quantitatively by a competitive ELISA. Participants were followed for 6 months after the final dose to identify confirmed SARS-CoV-2 infections. The cohort included 97 males (31%) and 216 females (69%), with a mean age of 39.43 years. The median SARS-CoV-2 IgG antibody level at day 28 was 7713.3 AU/mL, and the median neutralizing antibody inhibition rate was 99.2%. Antibody levels were not significantly associated with age or comorbidities. Booster vaccination induced a strong humoral immune response in all participants. However, the occurrence of post-vaccination infections despite high antibody levels suggests immune escape by emerging variants. While vaccines may not fully prevent infection, they provide substantial protection against severe disease and mortality.

Treat-to-target strategies have improved mucosal healing in inflammatory bowel disease; however, nearly half of patients in clinical remission still experience disabling fatigue. Morais et al published a study in the World Journal of Gastroenterology demonstrated that biologic treatment success does not necessarily improve patient-reported outcomes and fatigue cannot be explained solely by disease activity or conventional inflammatory biomarkers. A major strength of the study lies in its focus on fatigue as a primary clinical outcome. Although depression, anxiety, stress, and insomnia had limited predictive value individually, their combined assessment increased fatigue risk up to 45-fold. The composite psychological score demonstrated good discriminative performance, supporting its practical use in routine care. Fatigue was also associated with leukocyte alterations, such as relative neutrophilia and lymphopenia/eosinopenia, consistent with stress-related immune activation. No significant associations were found with anemia, nutritional deficiencies, thyroid function, or C-reactive protein, underscoring the multidimensional and largely inflammation-independent nature of fatigue in Crohn’s disease and highlighting the need for a more patient-centered management approach.

Celiac disease (CD) is a chronic, immune-mediated enteropathy triggered by dietary gluten in genetically susceptible individuals, most commonly those carrying human leukocyte antigen-DQ2 or human leukocyte antigen-DQ8 haplotypes. However, because these haplotypes are prevalent in the general population while only a minority of carriers develop disease, additional factors are likely to contribute to disease onset and progression. In recent years, the gut microbiota has emerged as a potential mediator between host genetic susceptibility and environmental triggers, particularly in pediatric CD. Current evidence suggests that children with CD exhibit reduced microbial diversity, depletion of beneficial commensals, enrichment of proinflammatory taxa, and broader alterations extending to fungal and viral communities. However, these findings remain heterogeneous, largely due to variability in study design, sampling sites, diet, age, and analytical methods. This review examines the interplay between host genetic risk and the intestinal microbiota in pediatric CD, with emphasis on bacterial, fungal, and viral components. Moreover, it highlights the importance of longitudinal, functionally oriented, and multi-omics approaches, particularly in genetically at-risk yet clinically unaffected children, to better clarify causality and identify early microbial markers of disease susceptibility.

IntroductionThis systematic review aimed to provide a comprehensive evaluation of the immunopathological mechanisms associated with SARS-CoV-2 infection and COVID-19 vaccination based on current evidence. Particular emphasis was placed on cytokine storm, endothelial dysfunction, complement activation, and autoimmune processes in COVID-19 pathogenesis.MethodsThe study was conducted as a systematic literature review in accordance with PRISMA guidelines. English-language research articles published between 2020 and 2026 were identified through a structured search of the Scopus database. A total of 1,331 records were screened, and 53 studies were included based on predefined inclusion and exclusion criteria. The findings were systematically categorized according to major immunopathological mechanisms.ResultsThe included studies indicate that endothelial dysfunction (24.5%) and cytokine dysregulation (18.9%) are the most frequently reported mechanisms in COVID-19 immunopathogenesis. Autoimmune responses (15.1%), complement activation (17%), and immune complex–mediated inflammation also play significant roles. Elevated levels of proinflammatory cytokines, lymphopenia, and markers of vascular injury were consistently associated with increased disease severity and mortality. In addition, persistent immunological alterations and autoantibody production were observed in a subset of patients during the post-COVID period.ConclusionCOVID-19 pathogenesis is driven by complex and interconnected immunopathological mechanisms rather than viral effects alone. Hyperinflammation, endothelial dysfunction, complement activation, and autoimmune processes are key determinants of disease severity and clinical outcomes. These findings underscore the importance of targeted immunomodulatory strategies and provide a comprehensive framework for future research.

Inflammatory bowel diseases (IBDs) are classified into two distinct types based on the area and severity of inflammation: Crohn's disease (CD) and ulcerative colitis. In CD, gut bacteria can infiltrate mesenteric fat, causing expansion known as creeping fat, which may limit bacterial spread and inflammation but can promote fibrosis. The gut bacteria composition varies depending on whether the colon or ileum is affected. Fecal microbiota transplantation (FMT) transfers feces from a healthy donor to restore gut microbiota balance, often used in IBD patients to reduce inflammation and promote mucosal repair. The use of FMT for CD remains uncertain, with insufficient evidence to fully endorse it as a definitive treatment. While some studies suggest it may improve symptoms, questions about the duration of these improvements and the need for repeated treatments persist. There is a pressing need for methods that provide long-term benefits, as highlighted by Wu et al 's research.

Tarihin başlangıcından beri birlikte yaşadığımız mikroorganizmalar belki de Dünya'nın kaderini sayısız kez etkilemiştir. Çiçek, veba, frengi, cüzzam, kolera gibi hastalıklar bunun en çarpıcı örneklerindendir. Yakın geçmişte yaşadığımız COVID-19 pandemisi ise Tıbbi Mikrobiyolojinin hayati önemini insanlığa bir kez daha güçlü bir şekilde hatırlatmıştır. Bu görünmez varlıklarla savaşta, mikrobiyolojinin derinlemesine anlaşılması ve uygulanması, gelecekte insan sağlığını korumanın anahtarı olacaktır. Son yıllarda gelişen moleküler yöntemlerle, mikroorganizmalar ve insan arasındaki karmaşık ilişki daha derinlemesine anlaşılmaya başlanmıştır. Günümüzde mikrobiyota, tüm tıp disiplinleri tarafından büyük bir ilgiyle incelenmekte ve önemli bir araştırma konusu olarak değerlendirilmektedir. Kuşkusuz, vücudumuzda yaşayan mikroorganizmaların etkileri sadece geleneksel enfeksiyon hastalıklarıyla sınırlı kalmamaktadır. Diyabet, obezite, Alzheimer ve bazı kanser türleri gibi klinik tabloların da mikroorganizmalarla bağlantılı olabileceği öne sürülmektedir. “Cumhuriyetin 100. Yılına 100 Kitap” Projesi kapsamında hazırlanan "Tıbbi Mikrobiyoloji” ders kitabı"nın, sağlık çalışanları ve öğrenciler için değerli bir kaynak olmasını temenni ediyoruz.

Advanced gastric cancer (GC) remains a high-mortality malignancy despite progress in diagnosis and treatment, including immunotherapy. Reliable prognostic markers are essential for better patient stratification. The triglyceride-glucose (TyG) index, a marker of insulin resistance, has shown promise in various cancers, but its role in GC remains unclear. Yao et al investigated its prognostic value in 300 patients with advanced GC receiving immunotherapy and chemotherapy. Their model, which integrates the TyG index, programmed death-ligand 1 expression, and Eastern Cooperative Oncology Group performance status, underscores the impact of metabolic dysfunction on immune response and treatment efficacy. This letter examines the TyG index's potential as a prognostic tool in GC and its implications for treatment strategies guided by metabolic and immune factors, as demonstrated in Yao et al research.

Introduction:It is suggested that Helicobacter pylori (Hp) can reach the brain via the oral-nasal-olfactory route, through Hp-infected monocytes in the disrupted blood-brain barrier (BBB), or through a rapid retrograde neural network leading to neurodegeneration from the gastrointestinal tract (GIS) and may lead to neurodegenerative diseases such as Alzheimer's (AD), Parkinson's (PD) and Multiple sclerosis (MS). In this study, we aimed to evaluate the possible immunopathogenesis relationship between Hp-specific antigens and neurodegenerative diseases by determining the frequency of seropositivity against different specific antigens of Hp in diseases such as AD, PD and MS. Methods:In our cross-sectional, retrospective case-control study, the immunoreactivity frequencies of Hp-specific and non-specific CagA (p120), VacA (p95), p75, FSH (p67), UreB (p66), HSP homolog (p57), flagellin (p54), p50, p41, p33, OMP (p30), UreA (p29), p26, OMP (p19), p17 antigens were determined by Western Blot method in 36 AD, 35 PD, 91 MS cases with Hp-IgG reactivity, and 55 controls without a neurodegenerative/demyelinating by ELISA method. Results:No significant difference was found between the immunoreactivity frequencies of Hp antigens between AD and control groups (p>0.05). In the multivariate logistic analysis performed for PD cases, age ≥ 50 and immunoreactivity frequency of p19 were found to be independent risk factors (OR: 36.752, p<0.05) (OR: 5.570, p<0.05). In MS cases, immunoreactivity frequency of p17 antigen was found to be a risk factor (OR: 2.646, p<0.05). In addition, the mean level of Hp-IgG reactivity was found to be negatively associated with MS development (indicating an inverse correlation) in the control group compared to the MS group (OR: 0.585, p < 0.05). Furthermore, logistic regression analysis in the total study group revealed that the immunoreactivity frequency of the p17 antigen was identified as a risk factor for MS (OR: 2.438, p<0.05). Conclusion:Our data on AD cases are insufficient. In PD cases, the significantly higher frequency of immunoreactivity to the Hp-p19 antigen in individuals aged ≥50 years (OR=5.570) is noteworthy. In the MS group, the significantly high detection of Hp p17 antigen and its presence as a risk factor (OR=2.646), and the significantly high detection of p26 antigen suggest the relationship between these antigens and the MS development process. However, it is a fact that new and many prospective cohort-based case-control studies are needed to reveal this more clearly.

Background: Crohn's disease (CD) and ulcerative colitis (UC) are inflammatory bowel diseases with uncertain etiology. We aimed to determine the amounts of Akkermansia muciniphila and Faecalibacterium prausnitzii in the intestinal microbiota of these patients and to correlate their amounts with blood IL-8, IL-10, and IL-12 cytokine levels. Methods: Thirty UC, 30 CDs, and 46 healthy controls were included. IL-8, IL-10, and IL-12 levels of blood samples were analyzed by ELISA. The amounts of Akkermansia muciniphila and Faecalibacterium prausnitzii were determined by the LightCycler 480 qPCR system. Results: F. prausnitzii, A. muciniphila, IL-10, and IL-12 decreased in patient groups, while IL-8 decreased in UC but increased in CD. A significant difference was detected between the patient and control groups in terms of F. prausnitzii, A. muciniphila, and IL-8, but not for others. The amount of F. prausnitzii was correlated with IL-8 and IL-10 in UC and with IL-10 in CD patients. Conclusions: The decrease in the amount of F. prausnitzii was associated with the increase in UC disease severity. A. muciniphila and F. prausnitzii were detected in lower amounts in both diseases. F. prausnitzii decreased more with the severity of UC, suggesting that these bacteria may have complex roles in their etiopathogenesis.

Objective: Chronic obstructive pulmonary disease (COPD) is described as partially reversible airflow limitation. P-glycoprotein (P-gp/MDR1), encoded by the Multidrug Resistance 1 (MDR1) gene, is regarded as a protective component for the respiratory tract and is present in tracheobronchial epithelium and lung parenchyma, and removes particles from cells and protects against various xenobiotics. Polymorphisms of MDR1 gene and the alteration in the expression of P-gp are considered to have a negative effect on the severity of COPD pathogenesis and treatment efficacy. We aimed to investigate the relationship of the MDR1 gene polymorphisms with reversibility in COPD patients. Materials and Methods: The MDR1 polymorphisms, specifically the 3435C>T and 2677A/G variations, were analyzed in 90 COPD patients. Results: 15 of the 90 COPD patients had positive reversibility tests. 2677TT (p=0.044) and 3435TT (p=0.003) alleles related to positive reversibility tests. There were no significant differences in the distribution of the MDR1 C3435 alleles and the G2677 alleles (p> 0.05). Conclusion: COPD patients with the TT allele have a higher rate of early reversibility positivity; this suggests that those carrying the allele may respond better to bronchodilator therapy. These markers could help to distinguish COPD patients who respond better to β2-agonists or who may not benefit much and, therefore, need different drugs.

Background: The coronavirus disease 2019 vaccine induces both antibody and T-cell immune responses and has been proven to be effective in preventing coronavirus disease 2019, including its severe disease form, in healthy individuals. However, the details of severe acute respiratory syndrome coronavirus-2 immunoglobulin-G antibody responses and severe acute respiratory syndrome coronavirus-2 specific T-cell responses in patients with sarcoidosis are unknown. Aim: To measure and compare antibody responses and T cell responses using enzyme-linked immunosorbent assays and interferon-gamma release assay in sarcoidosis patients infected with coronavirus disease 2019 and vaccinated with CoronaVac. Study Design: A prospective cohort study. Methods: A total of 28 coronavirus disease 2019 polymerase chain reaction test-positive sarcoidosis patients who were infected with severe acute respiratory syndrome coronavirus-2 in the past 6 months and did not have coronavirus disease 2019 vaccination and 28 sarcoidosis patients who were administered with 2 doses of CoronaVac and never had coronavirus disease 2019 were included in this study. The immune response levels of patients were determined by measuring the severe acute respiratory syndrome coronavirus-2 immunglobulinG and interferon-gamma levels in the blood of the patients by the enzyme-linked immunosorbent assays method and interferon-gamma release assay tests, respectively. Results: The mean age of the patients in the COVID-infected group was 48.1 ± 11.3, while the mean age of the patients in the vaccinated group was 55.6 ± 9.32. The mean time elapsed after infection was 97.32 ± 42.1 days, while 61.3 ± 28.7 days had passed since the second vaccination dose. In the COVID-infected group, immunoglobulin-G and interferon-gamma release tests were positive in 64.3% and 89.3% of the patients, respectively. In the vaccinated group, immunoglobulin-G was positive in 10.7% of the patients, and interferon-gamma release test was positive in 14.3%. Conclusion: Innate immune responses are better than adaptive immune responses in patients with sarcoidosis. The coronaVac vaccine is insufficient to generate humoral and cellular immunities in patients with sarcoidosis.

EDITORIAL article Front. Cell. Infect. Microbiol., 22 March 2023Sec. Microbiome in Health and Disease Volume 13 - 2023 | https://doi.org/10.3389/fcimb.2023.1187247

Background: The polymorphisms in the region between 58 and 62 amino acids of the 194-amino acid CagL protein (CagL hypervariable motif) affect the binding affinity of CagL to integrin α5β1 (ITGA5B1) receptor in host epithelial cells and have an effect on the development of various gastrointestinal diseases. We aimed to evaluate the associations of gastroduodenal pathologies, with the polymorphisms of cagL gene of Helicobacter pylori (H. pylori) and also associations between vacA genotypes and cagL polymorphisms. Methods: A total of 19 gastric cancer, 16 duodenal ulcer, and 26 non-ulcer dyspepsia patients were included in this case-control study. All cases had H. pylori. A fragment of 651 bp from gene cagL (hp0539) and cagA, vacA genes was amplified by polymerase chain reaction. Purified polymerase chain reaction products were sequenced by Sanger sequencing, and nucleotide sequences were translated into amino acid sequences. Results: All of the H. pylori strains had cagL and cagA genes. In the 16 (84%) gastric cancer cases, the D58 amino acid polymorphism was significant than the 4 (15.4%) duodenal ulcer cases (P = .029), and the D58/K59 amino acid polymorphism was significant in 12 (63.1%) of the gastric cancer cases than 1 (3.85%) duodenal ulcer case (P = .008). D58/K59 and DKIGQ (n = 10; 52.63%) were the most common polymorphisms in the gastric cancer and were associated with the vacA genotype s1/m2, respectively (P = .022 and P = .008). The D58/K59 amino acid polymorphism was found to have a significant Odds Ratio (OR) value of 8.9 (P = .0017) in multivariate logistic regression analysis. Conclusions: The risk of gastric cancer development is 8.9 times higher with D58/K59 polymorphism.

Background: HAdV-36 leads to adipocyte proliferation of adipose tissue through E4orf1 gene, leading to the development of obesity and related diseases. We aimed to investigate the presence and any association of HAdV-36 in non-alcoholic fatty liver disease (NAFLD) patients Methods: The patient group was composed of 116 patients; 30 obese patients with NAFLD (BMI > 30 kg/m2), 30 patients with Diabetes Mellitus (DM)+NAFLD (BMI > 30 kg/m2), 16 patients with NAFLD (BMI < 30 kg/m2), and operated obese group with NAFLD (BMI > 30 kg/m2). The control group comprised 81 non-obese healthy adults. Liver adipose tissue samples were obtained in 30 operated NAFLD patients. HAdV-36-DNA, HAdV-36 neutralizing antibodies, serum lipid, and adipokine levels were analyzed. Results: HAdV-36 neutralizing antibodies (HAdV-36 Ab-positive) were detected in 10/116 and 2/81 participants in the study and control groups, respectively; the difference was statistically significant (p < 0.005). LDL, total cholesterol but not adipokine levels were found to be significantly higher in HadV-36 Ab-positive patients (p < 0.05). While HAdV-36 was identified as a risk factor with OR = 4.11 in univariate analyses, there was no significant difference in binary logistic regression analysis. HAdV-36-DNA was detected in the adipose tissue samples of two patients. Conclusions: We suggest that the presence of HAdV-36 may lead to the development of obesity with the increase in adipose tissue, and diseases such as hyperlipidemia, NAFLD, DM, and metabolic syndrome may develop on the basis of chronic inflammation caused by obesity. Thus, HAdV-36 may be a plausible risk factor for the development of NAFLD.

In this study we describe how the hippocampus and subiculum act in concert to encode information in a spatial delayed-nonmatch-to-sample (DNMS) task. This encoding was functionally partitioned between neurons within subiculum and hippocampus to uniquely identify trial-specific information accounting for both spatial and temporal constraints on performance within and between trials. Encoding by subicular neurons in the task was normally accurate and specific, but only if delays were shorter than 15 s, whereas trial-specific information encoded by hippocampal neurons was subject to strong biases from prior trial sequences and was accessible only when delays exceeded 15 s. The two structures operated in a complementary manner to encode information correctly on 75% of all trials using the above strategies. The remaining 25% of trials were at risk due to inherent idiosyncrasies by which hippocampal and subicular neurons encoded information and became errors when the random sequence of trials conflicted with these constraints.

Objective Helicobacter pylori (Hp) and Epstein-Barr virus (EBV) are involved in gastric cancer (GC) etiology. EBV/Hp co- infection was thought synergistically increase gastroduodenal disease occurence. We aimed to determine the presence of EBV/Hp co-infection in gastroduodenal diseases. Methods The study group had 68 Hp (+) cases [25 GC, 13 IM (intestinal metaplasia), 30 PU (peptic ulcer)], and the control group had 40 NUD (non-ulcer dyspepsia) cases [20 Hp+, 20 Hp-]. EBV-DNA was detected by non-polymorphic EBNA-1 gene-based qPCR. EBV/EBNA-1 IgG levels were determined by quantitative and qualitative ELISA methods, respectively. Results EBV-DNA positivity was 32% (8/25), 6.6% (2/30) and 5% (1/20) in GC, PU and NUD Hp (+) cases, respectively. There was a significant difference (p = 0.001) between GC (32%) and NUD Hp (+) (5%) cases in terms of EBV-DNA positivity. Mean EBV-DNA copy numbers were 6568.54 ± 20351, 30.60 ± 159.88 and 13.85 ± 61.93 for GC, PU, and NUD, respectively. In terms of the mean EBV-DNA copy number, a significant difference was found between the groups (p = 0.005). In terms of EBV/EBNA-1 IgG antibody positivity, no significant difference was found between GC and NUD cases (p = 0.248). EBV DNA positivity was found to be significant (odds ration [OR] = 26.71 (p=0.009, %95CI 2.286- 312.041) in multivariate logistic regression. Conclusioin Although we had a small number of GC cases, it can be suggested that the estimated risk created by the synergistic effect based on the addition of EBV increased 26 times in the presence of Hp in GC.

Background: Monitoring the longevity of immunoglobulin G (IgG) responses following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infections is vital to understanding the role of antibodies in preventing infection. Aims: To determine the quantitative IgG responses specific to the Spike-S1 (S1) receptor-binding domain (S1/RBD) region of the virus in serum samples taken between 4 weeks and 7 months after polymerase chain reaction (PCR) positivity in patients who are diagnosed with coronavirus disease-2019 (COVID-19). Study Design: A longitudinal study. Methods: This study included 113 patients with a clinical and molecular diagnosis of COVID-19. The first and second serum samples were taken 1 and 7 months, respectively, after the PCR positivity. S1/RBD-specific IgG antibody response was assayed using anti-SARS-CoV-2 QuantiVac ELISA (IgG) kit (Euroimmun, Lübeck, Germany). The neutralizing antibodies were investigated in 57 patients whose IgG test results were above the cut-off value. Results: In 57 patients with SARS-CoV-2 IgG, the anti-SARS-CoV-2 IgG quantitative antibody levels significantly decreased after 7 months (Z = −2.197, p = 0.028). A correlation was detected between the anti-SARS-CoV-2 IgG and nAb percent inhibition (IH%) levels detected in 1 month (rs = 0.496, p < 0.001), but without significant correlation in serum samples taken on 7 months. The nAb IH% levels of the first and second were compared for COVID-19 severity and revealed no statistical difference (p = 0.256). In the second serum sample, the nAb IH%s of patients with moderate COVID-19 showed a statistically significant difference from patients with mild COVID-19 (p = 0.018), but without significant differences between severe and moderate or mild COVID-19. Conclusion: SARS-CoV-2 quantitative IgG antibody titers are significantly reduced at long-term follow-up (> 6 months). Due to the limited information on seroconversion, comprehensive studies should be conducted for long-term follow-up of the immune response against SARS-CoV-2.

This study aimed to determine the anti-S (receptor binding protein) RBD IgG antibody titers formed against Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2) and the neutralizing antibody inhibition percentages (nAb IH%) in blood samples taken after two doses of inactive or mRNA-based vaccine and a booster dose. Volunteers with two doses of inactivated CoronaVac (heterologous group; n = 75) and BioNTech (BNT)162b2 mRNA vaccine (homologous group; n = 75) were included in this study. All participants preferred the BNT162b2 vaccine as a booster dose. First, peripheral blood samples were taken 3 months after the second vaccine dose. Second, peripheral blood samples were taken 1 month after the booster dose. Anti-S-RBD IgG titers were determined by CMIA (SARS-CoV-2 IgG II Quant). Neutralizing antibodies were detected by a surrogate neutralization assay (SARS-CoV-2 NeutraLISA, Euroimmun, Lübeck, Germany). The median age of the volunteers was 40 (IQR 29–47) years old. After the heterologous booster dose, anti-S-RBD IgG levels and neutralizing antibodies increased approximately 50-fold and 9-fold, respectively. Anti-S-RBD IgG titers increased by 9 and 57 times, respectively, while nAb IH% increased by 1.5 and 16 times, respectively, among those with heterologous reminder doses and those with and without a prior history of coronavirus disease (COVID-19). This study showed that after the administration of a heterologous booster dose with BNT162b2 to those whose primary vaccination was with inactivated CoronaVac, the binding and neutralizing antibody levels were similar to those who received a homologous BNT162b2 booster dose. It was observed that the administration of heterologous and homologous booster doses resulted in the development of similar levels of neutralizing antibodies, independently from a prior history of COVID-19.

Objective: Control of corneal damage with endothelial cell count and serological screening before keratoplasty are critical issues for recipient health. We aimed to detect the pre-transplantation hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), and Treponema pallidum serological test results of post-mortem corneal donors and to determine their correlation with serological and molecular tests to support or verify low reactive/positive test results.Methods: The serological test results of post-mortem corneal donors sent from the eye bank between January 2015 and December 2020 were analyzed retrospectively, and demographic and serological test data of these donors were obtained from ELISA laboratory data by the ISHOP system Cerrahpaca Medical Faculty Hospital.Results: Of 424 post-mortem corneal donors, 161 (37.7%) were female, and 263 (62.03) were male; 13 (3.06%) had high HBsAg positivity, 23 (5.42%) had low anti-HCV reactivity, 19 (4.48%) had low anti-HIV 1/2 reactivity, and two (0.47%) had high Tp-Ab IgG reactivity. Therefore, the corneas of a 30-year-old woman with positive HCV RNA result and 13 donors with high titer HBsAg positivity, and two donors with high reactivity in the Tp-Ab IgG test were not eligible for the Eye Bank after performing a real-time PCR assay for the confirmation of donors with low reactivity.Conclusion: We believe that it is essential to apply serological tests pre-keratoplasty to prevent infection transmission and perform confirmatory tests in low positivity/reactivity that may occur due to post-mortem coagulum hemolysis, within the framework of a collective and specific algorithm.

BACKGROUND:Obesity may also develop due to a viral infection caused by adenovirus 36. We aimed to detect the presence of neutralizing antibodies against Ad-36 in adult patients who developed type 2 diabetes due to obesity (BMI ≥ 30 kg/m2). METHODS:The patient group (PG) was composed of 80 obese people with type 2 diabetes, the patient control group (PCG) was composed of 40 non-obese people with type 2 diabetes, and the healthy control group (HCG) was com-posed of 40 non-obese people without type 1 or type 2 diabetes in this case-control study. The presence of Ad-36 neutralizing antibodies was studied by serum neutralization assay. RESULTS:A significant difference was found between the PG and HCG in terms of Ad-36 antibody positivity (p < 0.0001) but no significant difference was detected between the PG and the PCG (p > 0.05). BMI, serum leptin, adiponectin, and triglyceride levels were significantly higher in the PG (p < 0.05). Conversely, TNF-α and IL-6 levels were significantly lower in the PG (p < 0.0001). When the two groups were compared, the mean levels of total cho-lesterol and LDL in the PG were found to be high, although not significant (p > 0.05). In type 2 diabetes patients (n = 120), age, BMI, HDL, LDL, triglyceride, total cholesterol, Ad-36 presence, leptin, adiponectin, TNF-α, and IL-6 parameters were taken as independent variables for logistic regression. While BMIs was found to be significant (odds ration [OR] = 2.358; p = 0.0001, 95% Cl 1.507 - 3.690, Ad-36 presence was found to be a significant (OR = 27.352; p = 0.003, 95% Cl 3.157 - 236.961). Our study showed that BMI and Ad-36 increase type 2 diabetes risk by 2.3 and 27.3-fold in the PG and PCG (type 2 diabetes patients) versus the HCG. There was also a significant difference between PCG and HCG. CONCLUSIONS:We suggest that Ad-36 seropositivity is also a risk factor for the development of type 2 diabetes independent of being obese.