Russian Journal of Infection and Immunity
ISSN (print): 2220-7619, ISSN (online): 2313-7398 Founders: Russian Association of Allergologists and Clinical Immunologists Saint-Petersburg Regional Branch, Saint-Petersburg Pasteur Institute, North-Western Department of Medical Sciences Editor-in-Chief: Areg A. Totolyan, academician of RAS, Doctor of Sc., Professor Frequency / Access: 6 issues per year / Open Included in: White List (3rd level), Higher Attestation Commission List, RISC, Scopus, Web of Science Core Collection
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Pathogenetic mechanisms of developing impaired innate and adaptive immunity in sepsis
The objective of this review was to highlight the problem of sepsis, the relevance of which is determined by the growing number of patients, the complexity of pathogenesis, and the difficulty of early diagnosis. Sepsis is a life-threatening severe dysfunction of internal organs caused by an infectious agent and occurring as a result of a complex interplay between proinflammatory and anti-inflammatory processes that can lead to multiple organ failure and death. This condition holds one of the leading places in morbidity and high mortality in surgical and intensive care units, and its prevalence has continued to steadily increase over the past years, especially among groups of patients with chronic diseases and weakened immunity. At different stages of pathogenesis, immune mechanisms act as both a generator of damage reactions and the main components of the body’s defense reactions. Sepsis begins with an exuberant inflammatory reaction, which can last for several days, and then pass into a more protracted immunosuppressive period, with the outcome largely depending on the patient’s immune system. The article focuses on understanding the role of developing disorders of innate and adaptive immunity in the pathogenesis of sepsis, their manifestations, mechanisms of immune dysfunction in septic conditions leading to impaired immune response. Bacteria that cause sepsis overcome the protective mechanisms of human immunity, which leads to the development of acute bacteremia, while the immunosuppression caused by pathogens leads to generalization of the process. Prominent bacteremia, increasing endotoxinemia due to generalization can lead to excessive activation of inflammatory, anti-inflammatory reactions and uncontrolled release of inflammatory mediators, damage to the body’s defense mechanisms, particularly, depletion of T cells, decreased expression of human leukocyte antigen (HLA)-DR on monocytes and induced uncontrolled apoptosis of neutrophils and adaptive immune cells. This leads to a worsening of sepsis course and further aggravation of immune homeostasis disorders as well as continuing enhancement of the systemic inflammatory response. Therefore, a deeper understanding of the immunological aspects of sepsis pathogenesis, which are behind the development and progression of this condition, is becoming an important part of clinical practice and is of great importance for its timely identification, improvement of treatment strategies, increase in patient favorable outcomes and lowering related mortality.
Copyright (c) 2025 Poryadin G.V., Zakhvatov A.N., Mosina L.M., Tarasova T.V., Haidar D.A., Saushev I.V., Tishkov P.S. https://creativecommons.org/licenses/by/4.0
Pathogenesis of autoimmune inflammation in COVID-19: a literature review
The literature review examines the mechanisms underlying formation of autoantibodies to angiotensin converting enzyme (ACE) in COVID-19. The similarity of the autoimmune processes revealed in the new coronavirus infection and the inflammatory reactions previously studied in experimental models is shown. Plausible ways for developing neurodegenerative and rheumatic diseases and rheumatic diseases in patients after a new coronavirus infection are presented. The results of clinical studies have shown that COVID-19 convalescent patients often have serum antibodies to ACE type 2 (ACE2-specific antibodies), which are absent in non-COVID-19 apparently healthy individuals. The authors note that higher level of such antibodies was paralleled with more severe COVID-19. ACE2 is known to catalyze the degradation of angiotensin I and angiotensin II, and also converts angiotensin II into angiotensin 1–7, which has vasodilating, anti-inflammatory, and antifibrotic effects. Accordingly, low ACE2 level along with anti-ACE2 antibodies imprints progression of inflammation and tissue fibrosis, which obviously markedly exacerbates the course of the infectious and inflammatory process and increases the severity of irreversible post-inflammatory changes. Intravenous administration of heterologous polyclonal antibodies against pulmonary ACE has been shown to cause acute fatal pulmonary edema. Autoantibodies to ACE2 cause a predisposition of patients with connective tissue diseases to constrictive vasculopathy, pulmonary arterial hypertension and persistent digital ischemia, which was noted in a number of patients with severe COVID-19. Thus, COVID-19 is a very complex process that involves not only classical infectious and inflammatory, but also autoimmune reactions in human body. COVID-19 severity depends on magnitude of internal organs and body systems impairment. Improper treatment can provoke or activate autoimmune processes, including rheumatic and neurodegenerative diseases, which should be taken into account when choosing treatment regimens, including cases of new SARS-CoV-2 variants. The information summarized in the literature review substantiates a need for using immunosuppressive therapy in case of deterioration in COVID-19 patients.
Copyright (c) 2025 Volkov A.V., Ruzhentsova T.A. https://creativecommons.org/licenses/by/4.0
CSF/serum ratios: modern approach to assess intrathecal response
CSF/serum ratios are the quotients of protein concentrations between the cerebrospinal fluid and blood serum. This method provides an objective assessment of proteins amount and origin in the cerebrospinal fluid. The cerebrospinal fluid protein composition consists of blood proteins passing through the blood-brain barrier and those synthesized within the central nervous system (intrathecally). Increased concentrations of proteins such as specific antibodies or autoantibodies in cerebrospinal fluid do not always mirror intrathecal synthesis or the presence of a pathological process in the intrathecal space. Elevated protein levels in the cerebrospinal fluid may be due to the higher blood protein influx through the blood-brain barrier. Quantification of CSF/Serum ratios according to German liquor specialist Hansotto Reiber allows distinguishing between blood and brain protein origin. This method is recognized as relevant for distinguishing between blood-derived and brain-derived protein fractions by the German Society for Liquor Diagnostics and Clinical Neurochemistry (Deutsche Gesellschaft für Liquordiagnostik und Klinische Neurochemie e.V.). The review is based on analyzing main literature databases (PubMed, CyberLeninka, Google Scholar, Scopus) and the latest publications on liquor diagnostics. Principles of CSF/Serum ratios, specific antibody indices calculation, and Reibergram structure are described. The classification of intrathecal inflammation and disease-related data patterns of immunoglobulin synthesis typical for diseases of the central and peripheral nervous system are presented. Thus, this literature review provides a detailed insight into the general principles of the modern approach for assessing cerebrospinal fluid protein composition and improves intrathecal humoral response comprehension. Additionally, the latest data on intrathecal immune response features in multiple sclerosis, neuromyelitis optica spectrum disorders, encephalitis associated with anti-MOG, anti-NMDAR antibodies, rheumatological diseases with CNS involvement, and neuroinfections are summarized.
Copyright (c) 2025 Deomkina A.M., Sayfullin R.F., Shakaryan A.K., Shamsheva O.V. https://creativecommons.org/licenses/by/4.0
Imaging techniques for studying virus–cell interactions: a review of current methods and challenges
Knowledge of virus-host cell interactions is central to the formulation of antiviral therapies and vaccines. Because of their nanoscale size and dynamic nature, viruses are inherently difficult objects to investigate. Virus characterization, such as imaging viral structures, intracellular viral trafficking, and infection molecular mechanisms, has relied heavily on sophisticated imaging approaches. Classical light microscopy imaging, such as fluorescence and super-resolution microscopy, provides information on viral entry, replication, and protein localization within living cells. Electron microscopy (EM) techniques, such as Transmission Electron Microscopy (TEM), Scanning Electron Microscopy (SEM), and Cryo-Electron Microscopy (Cryo-EM), provide high-resolution structural information on the viruses and their replication compartments. Advances in correlative imaging techniques, which include light and electron microscopy, have improved our ability to study virus-induced cellular changes in three dimensions. But in comparison to the earlier developments, it remains challenging in virus imaging: a compromise between resolution and sample preparation, restrictions in labeling methods, the challenge in imaging rapid virus-host interactions, and biosafety limitations for highly pathogenic viruses. Solutions to these types of issues will be provided with the newer techniques such as AI-powered imaging analysis, nanotechnology-based imaging probes, and cryo-electron tomography. This review covers the present imaging methods in virology, their utilities and limitations, as well as future prospects, with an emphasis on microscopy to discern the interaction of viruses with cells electron microscopy.
Copyright (c) 2025 Singh S., Jain S., Sharma S., Vasundhara D. https://creativecommons.org/licenses/by/4.0
Polymorphism of DNA repair system protein genes and its association with chronic viral hepatitis C
Hepatitis C is an infectious disease that causes liver inflammation and often leads to a chronic process. The genes encoding proteins involved in DNA repair systems participate in developing immune responses and inflammation, making them promising candidates for studying genetic predisposition to a wide range of common diseases, including infections. However, this group of genes is rarely studied to assess their role in genetic susceptibility to infectious diseases. In the present study, we investigated a role for polymorphisms in DNA repair system protein genes (ATM (rs189037 and rs1801516), NBN (rs709816 and rs1805800), MRE11 (rs473297), TP53BP1 (rs560191), MLH1 (rs1799977), PMS2 (rs1805321)) in the pathogenesis of chronic hepatitis C. As a result, associations were found both between some studied markers (rs1805321 in the PMS2 gene and rs1801516 in the ATM gene) and chronic hepatitis C as well as relations of various quantitative traits and the polymorphisms of these genes. For example, variability in blood biochemical parameters (levels of cholesterol, glucose, iron, prothrombin index values, and thymol test results) was shown to depend on genotypes of two markers in the NBN gene (rs709816 and rs1805800). Clinical and morphological indicators are associated with variants in the NBN (rs1805800), MRE11 (rs473297), and PMS2 (rs1805321) genes. The absolute and relative levels of neutrophils are influenced by rs1805800 (NBN), rs473297 (MRE11), and rs1799977 (MLH1), whereas lymphocyte counts are affected by both markers in the NBN gene, rs473297 (MRE11), rs1799977 (MLH1), and rs1805321 (PMS2). The lowest post-treatment IgG levels are observed in carriers of rarer genotypes in rs1805800 and rs709816 in NBN gene. Thus, our study demonstrates an impact of the studied genes on the pathogenesis of chronic hepatitis C, although the mechanism underlying such associations is not always clear. Nevertheless, our findings suggest about pleiotropic effects of DNA repair protein genes and their involvement in developing chronic hepatitis C.
Copyright (c) 2025 Babushkina N.P., Shavrak V.E., Goncharova I.A., Beloborodova E.V. https://creativecommons.org/licenses/by/4.0
Deciphering crucial genes in pelvic inflammatory disease and their relationship with infertility through systems biology studies
Background. Pelvic inflammatory disease (PID) is an infection of the female reproductive system. PID is usually caused by infection with Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG). Women with PID have an increased risk of becoming infertility. The aim of this study was to determine the molecular mechanisms that influence infertility and embryonic development in PID with CT and NG infections. Materials and methods. Microarray data were extracted from the Gene Expression Omnibus (GEO), and the protein-protein interaction network was constructed using Cytoscape software. Network analysis was performed to identify hub-bottlenecks and sub-networks. The functional mechanisms for critical genes were identified using the webgestalt server. Results. RPL13, EEF1G, JAK2, MYC, IL7R, CD74, IMPDH2, and NFAT5 were identified as crucial genes in protein-protein interactions and gene regulatory networks in CT and NG infections of PID. Ribosome, hematopoietic cell lineage, platelet activation, and Chagas disease, JAK-STAT pathway, eukaryotic translation elongation, Rap1 pathway, apoptosis, protein processing in the endoplasmic reticulum, progesterone-mediated oocyte maturation, and Epstein–Barr virus infection were identified as significant signaling pathways involving in CT and NG infections. Conclusion. Our model suggests novel critical genes, and functional pathways involved in CT and NG infections, establishing a link between these infections and infertility. However, further studies in vitro and in vivo are needed.
Copyright (c) 2025 Saberi F., Dehghan Z., Pilehchi T., Mehdinejadiani S., Taheri Z., Zali H. https://creativecommons.org/licenses/by/4.0
The chronic inflammatory landscape in HIV infection: characteristics of innate immunity factors
HIV infection, despite the success of antiretroviral therapy, remains a pressing problem to study. In a number of patients, despite achieving control and undetectable viral load, the expected recovery of immunologic surveillance and adequate interaction of innate factors are not achieved. The aim of the present study was to comparatively evaluate the state of innate immunity factors in patients with HIV infection. Materials and methods. 2 main groups were formed consisting of 56 subjects with HIV infection — with undetectable viral load and with detectable viral load. The control group contained 20 age- and sex-matched apparently healthy volunteers. Serum innate immunity factors were assessed using Bio-Plex Pro Human Cytokine Screening Panel, 48-Plex (Bio-Rad Laboratories, Inc., USA). Results. The levels of IL-15, IL-5, VEGF were below the sensitivity threshold of the applied test-system across entire examined cohort, also observed for beta-NGF level in control group. Among all investigated indices in control group only a few of them showed insignificant differences with patients from main groups: IL-12p40, IL-13, IL-3, LIF, M-CSF, MCP-3. The general change pattern in most major cytokine levels consisted in significant hypercytokinemia in main group vs control group excepting for opposite difference for level of IL-2, TNFβ, IFNα2, G-CSF, IL-2Rα. Serum levels of Eotaxin, IL-17, IL-2Rα, IL-4 did not differ between control group and patients with viremia. Significant differences between subjects from main groups were recorded in the levels of IL-2Rα, IL-8, IP-10, MCP-1, MIG. The study confirmed the persistence of a prominent imbalance of innate immunity factors in patients with HIV infection, both in remission and in case of viral load. The chronic inflammatory landscape formed during HIV infection may be an important pathogenetic link for developing complications and syndromes associated with HIV infection.
Copyright (c) 2025 Knysh S.V., Markelova E.V., Kuznetsov A.S., Gorelova I.S. https://creativecommons.org/licenses/by/4.0
Influence of excessive pro-inflammatory immune response on immunological parameters in women with early miscarriages
The study results showed that in the early pregnancy (up to 12 weeks) in women with a full-term pregnancy, but suffering from genital infections, changes occur in cellular immune arm. Such alterations affect both innate and adaptive immunity due to activated inflammatory reactions. At the same time, despite detected infection, pregnancy in such women may progression without serious disturbances. However, studies have shown that much more prominent changes in immune system are observed in women with former miscarriages, if they also suffer from genital infections. In women with miscarriages paralleled with genital infections, changes in the immune system are more pronounced that may be accounted for by ongoing immune response hyperreactivity. The latter is referred to an excessive reaction of the immune system to ongoing infection that results in higher inflammation. Such excessive inflammatory processes can cause a disrupted normal mechanisms of pregnancy maintenance, which in turn contributes to increased risk of pregnancy termination, as is observed in miscarriages. In addition, a more pronounced imbalance between pro-inflammatory and anti-inflammatory interleukins is observed in women with miscarriage. Pro-inflammatory interleukins (such as IL-6, IL-1β) potentiate inflammation and may increase the risk of complications during pregnancy, including miscarriage. Anti-inflammatory interleukins, on the other hand, should maintain balance in immune system and counter inflammation, but in case of women with former miscarriage, their activity is insufficient to counteract infection-related inflammatory processes. Thus, the presence of genital infections in women with former miscarriage often leads to excessive immune system activity, which contributes to increased inflammation and disrupted physiological processes that support pregnancy. In such cases, immune response is inadequate and exuberant that may contribute to pregnancy loss.
Copyright (c) 2025 Aleynik V.A., Zhuraeva M.A., Mukhitdinova K.O., Babich S.M., Negmatshayeva X.N. https://creativecommons.org/licenses/by/4.0
Serotonin-related immunomodulatory effect in a model of a contaminated wound in warm-blooded animals
Introduction. The treatment of contaminated wounds remains a significant challenge, and the solution to this problem may lie in the realm of pathogenetic therapy. The aim of this study was to investigate serotonin-related immunoregulatory effects in a contaminated wound model in experimental animals. Materials and methods. Wistar rats underwent surgical skin incisions in the epigastric region along the abdominal white line. Control animals received intraperitoneal saline (1st group) injections. Experimental animals were administered serotonin (days 0–5) at a dosage of 1.43 mg/kg b.w. intraperitoneally (2nd group); a serotonin pulse therapy (1.43; 1.43; 3.58; 7.15; 14.30 mg/kg) regimen was also administered (3rd group). After 5 days, the animals were euthanized, and microbiological, immunological, and histological analyses were performed. Results. Upon serotonin treatment, total microbial wound and peri-wound contamination (both hemolytic and non-hemolytic) decreased by 27% compared to control group (p > 0.05). The number of yeast-like and mold-like fungi also decreased significantly in experimental groups, by 4 times in the low dose group (1.43 mg/kg/day) and 4.6 times after pulse therapy. At the same time, an immunomodulatory effect was noted presented as increased neutrophil phagocytic activity, IL-6 levels, and activation of granulocyte lineage in the hematopoietic system. Histological analysis revealed accelerated skin regeneration in groups of treated animals. Conclusion. Serotonin administration has an immunomodulatory effect in a model of contaminated wounds in animals, leading to reduced bacterial contamination and accelerated wound healing.
Copyright (c) 2025 Chibirova T.T., Skupnevskii S.V., Saveljev R.V., Kokaev R.I. https://creativecommons.org/licenses/by/4.0
Assessment of the ability of SARS-CoV-2 strains of genetic variants B.1.1 and JN.1 to evade neutralizing antibodies from 2020 and 2023 convalescent patients
Introduction. The SARS-CoV-2 virus is a highly variable pathogen accounted for by random mutations leading to the emergence of new genetic variants. Natural selection of SARS-CoV-2 variants is, among other things, the result of population level immunity impact. To predict the effectiveness of counteracting COVID-19 spread, it is necessary to study a potential for human immunity pre-formed against current virus strains to resist SARS-CoV-2 variants of concern for assessing ability of new genetic variants to escape the neutralizing antibodies to previously circulating variants pressure. The aim of the study was to compare neutralizing antibody titers in 2020 and 2023 COVID-19 convalescent patients to SARS-CoV-2 B.1.1 and JN.1 genetic variants strains. Materials and methods. Blood sera from 76 and 68 convalescent subjects, respectively, for 2020- and 2023-years samples were collected and stored at –70°C until used. The antibody titer was measured by neutralizing virus cytopathic effect in sensitive monolayer cell culture using test serum. The neutralizing activity of the sera was analyzed for two variants of SARS-CoV-2 VOC, Wuhan and Omicron. The statistical significance of the difference in antibody titers was assessed using the F-test; the difference was considered significant at p < 0.01. Results. The differences in neutralizing titer levels were significant between all four samples: 2020 sera against JN.1, 2023 sera against JN.1, 2020 sera against B.1.1, and 2023 sera against B.1.1. Conclusion. Antigenic changes allow the current JN.1 variant to evade the effects of neutralizing antibodies developed against strains of previous genetic variants in some cases. The 2023 samples showed higher antibody titers in neutralizing strains of the old genetic variant B.1.1 due to repeated stimulation during vaccinations and reinfection. Spontaneous mutations being not crucial did not lead to changes in antigenic determinants critical for virus neutralization. Repeated contacts with altered genetic variants of SARS-CoV-2 increased protection against its parental wild type.
Copyright (c) 2025 Pyankov S.A., Zaykovskaya A.V., Rybel A.V., Bodnev S.A., Pyankov O.V. https://creativecommons.org/licenses/by/4.0
Blood plasma сytokine levels in patients with chronic viral hepatitis B stage-dependent liver fibrosis
Introduction. Hepatitis B is an infectious inflammatory liver disease resulting from hepatitis B virus infection. According to the WHO estimates, 254 million people with chronic hepatitis B (CHB) were recorded worldwide in 2022. CHB is accompanied by developing liver fibrosis, which leads to impaired liver function. The progression of liver fibrosis involves multilayered cellular interactions between hepatic stellate cells, resident macrophages, and specialized immune cells. this cell interplay is regulated by humoral factors, among which cytokines play a key role. Due to this, the analysis of peripheral blood cytokines in CHB patients allows assessment of immune process activity in the liver, fibrosis progression intensity, and therapeutic effectiveness. The aim of our work was to evaluate blood plasma cytokine spectrum in CHB patients related to liver fibrosis staging. Materials and methods. The study included 53 patients diagnosed with chronic viral hepatitis B, subdivided into three groups based on liver fibrosis stage. Blood plasma samples were collected from all study subjects. Concentration for 42 cytokines was assessed by xMAP multiplexing technology. The results underwent statistical processing using nonparametric statistical methods. Results. Compared to apparently healthy group, CHB patients showed: significantly elevated concentrations for IL-6, IL-27, CCL11/Eotaxin, CXCL9/MIG, CXCL-10/IP-10, M-CSF; significantly decreased levels for IL-2, IL-4, IL-12(p70), IL-13, IL-17A, IFN2α, sCD40L, CCL3/MIP-1α, CCL7/MCP-3, CXCL1/GROα, CXCL8/IL-8, CX3CL1/ Fractalkine, EGF, PDGF-AA, PDGF-AB/BB, VEGF-A. Based on different liver fibrosis stages, significant differences in cytokine levels were found between patient groups for: IL-6, IL-10, IL-12(p70), IL-27, sCD40L, CXCL9/MIG, CXCL-10/IP-10, M-CSF, PDGF-AA, PDGF-AB/BB. Correlation analysis revealed a positive relationship between liver fibrosis severity and levels for IL-6, IL-27, TNFα, CXCL8/IL-8, CXCL9/MIG, CXCL10/IP-10, and M-CSF, and a negative relationship between the severity of liver fibrosis and levels for IL-12(p70), IFN2α, sCD40L, CX3CL1/Fractalkine, EGF, PDGF-AA and PDGF-AB/BB. Thus, blood plasma cytokine spectrum in CHB patients was evaluated, identifying factors involved in CHB immunopathogenesis, including those playing a significant role for developing liver fibrosis.
Copyright (c) 2025 Batsunov O.K., Arsentieva N.A., Liubimova N.E., Duong D., Basina V.V., Esaulenko E.V., Totolian A.A. https://creativecommons.org/licenses/by/4.0
Analysis of post-vaccination immune resilience against hepatitis B healthcare workers of the Republic of Tatarstan
The aim of our study was to investigate the duration and resilience of HBV post-vaccination humoral immunity in healthcare workers of the Republic of Tatarstan. Materials and methods. Blood serum samples collected from 212 medical workers of the Republic of Tatarstan by assessing anti-HBs antibody level using ELISA with certified commercial test systems manufactured by JSC “Vector-Best”. Statistical analysis and visualization of the obtained data were performed using the Microsoft Office Excel and StatTech v. 4.1.5 (Russia). Results. The analysis showed that 42.5% of medical workers had no protective HBV antibody level at the time of the survey. Among seropositive individuals, every fifth medical worker had a low titer of anti-HBs IgG. The most vulnerable group turned out to be subjects aged 40–49 because they were found to have peak number of seronegative individuals — 59.7%. With increasing post-vaccination length, the percentage of subjects lacking protective HBV antibody titer became elevated. Whereas 62% of healthcare workers had a protective titer five years after completed vaccination course, only 55.3% of those examined here remained seropositive 10 years afterwards. Assessing a relationship between resilience of age-related post-vaccination immunity at the time of vaccination confirmed the statement that the older the age at which vaccination was begun, the more often individuals with low titers of protective HBV antibodies were found. Conclusion. The study data on resilience and duration of hepatitis B post-vaccination immunity in healthcare workers evidence that slightly more than half of those examined had protective HBV antibody titers. With increasing age, the resilience of HBV immunity wanes. To prevent nosocomial infection of medical personnel, it is necessary to assess time-dependent resilience and duration of HBV post-vaccination immunity. At the same time, we believe that only individuals with low anti-HBs IgG levels should be subject to annual testing for decision-making on applying booster dose vaccination. Revaccination should be carried out taking into account the individual characteristics of each vaccinated person. Given that HBV vaccination showed age-related effectiveness, we agree with the WHO statement clarifying that vaccination should begin as early as possible in childhood, with subsequent “catch-up” vaccination in adolescents and adults.
Copyright (c) 2025 Lokotkova A.I., Mamkeev E.H., Galiullina A.I., Iskandarov I.R., Galeev A.D., Lokotkova K.V. https://creativecommons.org/licenses/by/4.0
The state of humoral immunity to measles, rubella and mumps in healthy people and patients with measles
Measles, rubella and mumps are viral infections that can be prevented with highly effective vaccines. Recently, the incidence of measles and mumps has increased in many countries, involving highly immunized populations. The aim of the study was to assess measles, rubella and mumps humoral immunity in healthy people of different ages and compare these data with measles incidence in same area during the same time period. The serum samples from 713 conditionally healthy residents of different ages from Moscow and the Moscow region with an unknown vaccination history and from 700 patients with measles collected on the 4th-5th day after onset of rash were examined. Humoral immunity was determined by ELISA using the kits from Vector-Best (Russian Federation) and Euroimmun (Germany). It was found that in the group of 1–5-year-old subjects, the seropositivity rate was below 60%. Seroprevalence in groups over 6-year-old subjects against rubella fluctuates at the level of 87–94%, mumps — 72–83%. The most unstable situation was observed in humoral immunity against measles virus. In the group of 6–13-year-old subjects, seroprevalence increased to 79% followed by decline to 49.5% in group of 18–30-year-old subjects. The subsequent increase in seropositivity to 88.12% in the group over 51-year-old subjects was significantly lower than the calculated population immunity level (95%). Among measles patients in 2024, children and adolescents accounted for 54.32%. Comparison of measles incidence with the measles seronegative level in the same age groups revealed a clear pattern: the more seronegative were subjects, the higher measles incidence was in this group. In a similar study on measles incidence in 2013, all children and adolescents responded to the infection with a primary immune response, and among adult patients, a secondary immune response was detected in 12–18%. In 2024, among children and adolescents with measles, 9–12% responded with a secondary immune response, and in adult groups, the proportion of secondary response reached 44%, indicating that individuals vaccinated in childhood but who lost measles antibodies during life actively contribute to measles cases. Vaccination of seronegative grades 10–11 adolescents is necessary.
Copyright (c) 2025 Zherdeva P.E., Toptygina A.P., Nozdracheva A.V., Mamaeva T.A., Novikova L.I., Smerdova M.A., Iаrmolskaia M.S., Dementeva N.G., Gotvyanskay T.P., Semenenko A.V. https://creativecommons.org/licenses/by/4.0
Detection and phylogenetic analysis of Clostridium ventriculi in autistic children
Background. Autism spectrum disorder (ASD) is characterized by repetitive behaviors. There is evidence that gut flora imbalance may cause GI difficulties in autistic people. Gastrointestinal (GI) issues are associated with Clostridium ventriculi (C. ventriculi). The aim of this study was to use 16S rRNA gene sequencing to identify and genetically describe Clostridium ventriculi in fecal samples from children with autism. Materials and methods. A case-control study was done on fecal samples collected from 50 children diagnosed with autism. Also, samples were taken from 50 children who were not autistic as a control group. Using the FavorPrep Genomic DNA Mini Kit, DNA was extracted. PCR was used to amplify the 16S rRNA gene using the universal primers 27F and 1492R. After the PCR products were sequenced, BLAST and BioEdit tools were used to check the sequences for homology. The MEGA program was used for phylogenetic analysis. Results. Based on PCR results, 10% (5/50) of the 50 samples of autistic children that were examined proved positive for C. ventriculi, and all control group were negative for this bacteria. Genetic polymorphisms were indicated by specific nucleotide transitions and transversions that were discovered by sequencing. The Iraqi isolates and global samples exhibited a high level of genetic similarity (99%) according to phylogenetic analysis, indicating a recent common ancestor and potential clonal expansion. Conclusion. The discovery of C. ventriculi in autistic children raises the possibility of a connection between this bacteria and gastrointestinal problems linked to ASD.
Copyright (c) 2025 Hasan A., Lazim H. https://creativecommons.org/licenses/by/4.0
Measles morbidity in the Northwestern Federal District of the Russian Federation
Introduction. The COVID-19 pandemic profoundly affected measles epidemic process. On the territory of the Russian Federation, restrictive measures contributed to the continuation of measles circulation, but the pandemic created the prerequisites for further development of outbreaks. We have to analyze measles morbidity in the Northwestern Federal District in the pre- and post-COVID-19 period. Material and methods. Blood serum samples (n = 3179) collected from patients with maculopapular rash and fever were studied using ELISA. Results. In the Russian Federation in the years 2008–2010 measles incidence remained at extremely low level due to the importation of measles virus of different genotypes from global regions. In the territories of the Northwestern Federal District, during the period preceding the COVID-19 pandemic, measles incidence was characterized as sporadic. A major measles outbreak occurred in 2018–2019, with the disease being recorded in 6 of the 11 territories of the Northwestern Federal District. Since the introduction of quarantine measures, the number of verified measles cases has dropped sharply. The last case of measles in the region was reported in May 2020. In 2021, measles was not recorded in the territories of the Northwestern Federal District. The rise in measles incidence began at the late 2022 due to imported measles from Tajikistan. In 2023, measles incidence in the district amounted to 2.5 per 100 000 population. Measles continued to spread in 2024. In 2023 and 2024, the disease occurred mainly in unvaccinated subjects or those with unknown vaccination history; mostly children. The spread of measles in the territories of the Northwestern Federal District in 2022 and early 2023 was facilitated by late diagnosis and isolation of the first measles patients; introduction of measles into population groups not vaccinated against measles; delays in the supply of vaccines for populational immunization, including in outbreak areas. In general, measles circulation has resumed in the territories of the Northwestern Federal District.
Copyright (c) 2025 Antipova A.Y., Zheleznova N.V., Tolstykh N.А., Kaziakhmedova V.V., Gorziy E.S., Blokhinova M.A., Dumcheva O.S., Smirnova N.A., Zorina D.M., Molchanova Z.R., Buts L.V., Koltsov N.S., Dzhusoeva A.T., Dedkova L.S., Abramovskaya E.I., Smirnova I.K., Kalinina E.L., Gvozdeva I.S., Slepukhina N.L., Petukhova M.B., Gritsai A.B., Kozhemyakina M.A., Mironova A.V., Dedkov V.G. https://creativecommons.org/licenses/by/4.0
Molecular investigation of Proteus vulgaris virulence genes from asymptomatic bacteriuria in pregnant women
Background. It is a well-known bacterium Proteus vulgaris that causes urinary tract infections specifically bacteriuria. This study aimed to genetically search for the role of some virulence genes in this bacterium via bacteriuria in pregnant women of the Thi-Qar Governorate of Iraq. Materials anm methods. A mid-stream urine specimen with a total of 235 specimens was gleaned from pregnant women, which were performed in a random manner from various hospitals, when 116 cases suffered from UTI (patient group). The others (119 specimens) were collected from married women, but not pregnant women, and apparently in healthy cases (control group). MacConkey agar and blood agar were used for culturing and identification of bacteria under aerobic conditions, followed by microscopic examination, appearance description, biochemical test, API 20E analysis, and PCR analysis. Results. Genetic analysis revealed bacteriuria in 39 (33.6%) pregnant women infected with Proteus sp., but it stooped to 3 (2.5%) in apparently healthy women (control). When phenotypically and genotypically with specific identification genes of P. vulgaris the same samples were infected with this bacterium in eight (6.8%), while it receded to 1 (0.84%) in the control. The PCR and statistical analyses demonstrated that the total existence of each study gene (ureC, mrpA, and zapA) in bacteriuria isolates of P. vulgaris was 11/9 (122.2%), 9/9 (100%) and 9/9 (100%), respectively. There was significant variation in the position of zapA on chromosomes 8/9 (88.8%) and on the plasmid that was dropped to 1/9 (11.1%). Conclusion. The role of these bacteria is serious and significant in pathogenicity and attachment to the epithelial tissues of the urinary tract, the opportunistic nature of P. vulgaris, biofilm production, and elevated urine pH, which lead to stone production in pregnant women. PCR is the fastest and most accurate method for diagnosing P. vulgaris and its virulence genes.
Copyright (c) 2025 Ghali Jabur S. https://creativecommons.org/licenses/by/4.0
Biological properties of Klebsiella pneumoniae with classical and hypermucoid phenotype isolated from intensive care unit patients
Introduction. There are conflicting data on the biological properties of hypermucoid Klebsiella pneumoniae, so in practice there are difficulties in differentiating their pathotype. The aim of the study was to compare phenotypic properties for subpopulations of hypermucoid and classical K. pneumoniae isolated from intensive care unit patients. Materials and methods. The main group (n = 24) consisted of patients with hypermucoid K. pneumoniae, the control group (n = 24) consisted of patients infected with classical klebsiella. Isolation of K. pneumoniae from different biomaterial sources was performed by bacteriological method, identification — with “ErbaScan” microbiological analyzer using “Entero-Rapid 24” (Erba Lachema, Czech Republic). Lipase production was studied on Tributryn Agar Base (HIMEDIA, India), protease — on Micro-GELATINase (NICF, St. Petersburg), hemolysins — on 5% blood MPA (FBUN GSC PMB, Obolensk), presence of extended-spectrum β-lactamases (ESBLs) was investigated by the double-disc method, and sensitivity to phages by the SPOT test. Parametric and nonparametric statistical methods were used to process the data. The differences were considered significant at p < 0.05. Results. The detection rate of K. pneumoniae with a hypermucoid phenotype in intensive care unit patients was 23.1%; in 66.7% of cases these bacteria were isolated from sputum. Hypermucoid K. pneumoniae had a similar frequency of virulence factors production such as lipase (70.8% and 54.2%, respectively; p = 0.927), hemolysins (45.8% and 50%, respectively; p = 0.773), proteases (12.5% and 33.3%, respectively; p = 0.086). In hypermucoid and classical klebsiella, there were no differences in the frequency of ESBLs production (75% and 62.5%, respectively; OR = 1.8; 95% CI 0.521–6.218, p = 0.351) and the frequency of bacteriophage resistance (p > 0.05). In infectious processes associated with hypermucoid klebsiella strains, the level of patient leukocytes was significantly lower than in case of classical klebsiella infections (9.7 × 109 l vs 11.6 × 109 l; p = 0.028). However, regardless of the pathogen phenotype, patients had similar lengths of stay in the intensive care unit (12.5–16 days; p = 0.29) and mortality rates (58.2–62.5%; p = 0.77). Conclusion. Hypermucoid K. pneumoniae show a similar frequency of producing invasion factors, extended-spectrum beta-lactamases, and bacteriophage resistance to classical strains, which determines common approaches in the treatment of patients. The hypermucoid phenotype of bacteria is associated with lower levels of leukocytes, which must be taken into account to assess infection severity in patients.
Copyright (c) 2025 Isaenko O.A., Zakharova Y.V., Kuprienko T.S. https://creativecommons.org/licenses/by/4.0
Synergism and antagonism in intestinal microbial communities in closed organized collectives
Introduction. The gut microbiota represents the largest part of the entire human microbiome. The formation of a stable microbiota begins at childbirth, continuing to change during life influenced by various exogenous and hereditary factors. One of such external cues is presented by closed organized collectives, where different individuals, due to the common way of life and nutrition, undergo a restructuring of the intestinal microbial communities. In addition to microbiota quantitative and qualitative changes, inter-microbial communities may also be altered (synergism, antagonism, mutualism). The aim of the study was to analyze the synergistic and antagonistic relationships between intestinal microbial communities in individuals from closed organized collectives. Materials and methods. The study group included 120 male subjects aged 18 to 22 years, who lived within the same closed organized collectives for 9 months. Fecal samples were selected for plating prior to living in closed organized collectives (stage 1), and 9 months afterwards (stage 2). The identified microorganisms were assigned to the permanent, supplementary, or random microbiota group. To assess the relationship between pairs of genera, the Jaccard index was calculated. Results. The results of the study showed that the synergistic relationships between members of the permanent microbiota remain stable or increase over time, which generally corresponds to the data on the properties of the obligate microbiota. Positive synergistic relationships with additional microbiota have also been identified, e.g., between Bifidobacterium spp. and the order of Lactobacillales. The synergy of these genera can effectively support normal gastrointestinal tract functioning. However, antagonistic relationships were also noted, especially between some representatives of the additional and permanent microbiota, such as Klebsiella spp. Such data may indicate a negative effect of certain microorganisms on the intestinal microbiota in a limited collective setting. Conclusion. Further research in this field may help explain changes in microbial communities in organized collectives and develop strategies for healthy microbiota maintenance therein.
Copyright (c) 2025 Ermolaev A.В., Kaiumov K.A., Lyamin A.V., Gorbachev D.O. https://creativecommons.org/licenses/by/4.0
The gut microbiota features of patients with type 1 myocardial infarction with ST segment elevation
The relationship between the colonic biocenosis and the cardiovascular system is a relevant issue that has been thoroughly studied over the past 20 years. Nowadays, it has been proven that the intestinal microflora is able to regulate many host mechanisms, and its quantitative and qualitative changes trigger a cascade of pathological reactions. The main points of application through which the pathological effect is enabled are stimulation of systemic inflammation and lipid metabolism. Type 1 myocardial infarction with ST-segment elevation (STEMI) is the most dangerous form of coronary heart disease, often leading to death and disability. The aim of the study was to identify the features that determine the intraluminal colonic microbiota in patients with type 1 STEMI and estimate blood serum CRP level. The study enrolled 43 patients with type 1 STEMI aged 37 to 59 years. The first portion of feces was collected from and analyzed in patients with STEMI from the onset of clinical manifestations of the cardiovascular event. The control group consisted of age-matched conditionally healthy individuals (n = 41) without a history of ACS. Patients with STEMI are characterized by a reduced number of Bifidobacterium spp., Enterococcus spp. and typical E. coli strains. In main group, non-motile strain of E. coli, Staphylococcus spp. and opportunistic bacteria, especially representatives of the genera Citrobacter and Kluyvera, were more common. In addition, 76% of patients in main group had leukocytosis and absolute monocytosis, and 100% of cases had elevated CRP levels. Thus, the clinical study presents data reflecting the taxonomic characteristics of colonic microbiota in patients with type 1 STEMI and their inflammatory profile. Dynamic observation of such patients seems promising for the long-term assessing interplay between intestinal microbiocenosis, cardiovascular continuum, and human immune system.
Copyright (c) 2025 Stepanov M.S., Karpunina N.S., Godovalov A.P., Ipatova N.V. https://creativecommons.org/licenses/by/4.0
Assessing the effect of ultraviolet radiation on the mucosal microbiota of the alveolar processes in patients before dental implantation
Peri-implantitis is one of the most common complications during dental implant installation, occuring in 10–20% cases. The main cause for such complication is the production of biofilms by bacteria colonizing the implant placement area. The triggering factor for this is dysbiosis of the commensal oral flora. Studies show that Streptococcus spp. in association with Rothia spp., Neisseria spp., Corynebacterium spp. is normally found in healthy peri-implant sulcus However, in some cases Streptococcus spp. are indicator microbiota representatives in developing peri-implantitis. Ultraviolet radiation (UV) has been actively used in dental manipulations. The aim of the study was to analyze changes in the mucosa microbiota composition in alveolar processes of the upper and lower jaws upon exposure to UV radiation. Biopsies of mucosa collected from 35 patients, applied for dental implantation, were examined. Two mucosal samples were obtained from each patient. One of either sample was treated with a “Solnyshko” UV irradiator, the second sample remained intact. As a result of the study, 60 species of microorganisms were identified divided into the following groups: the group of constant microbiota, additional microbiota, transient microbiota. The constant microbiota for both samples before and after UV treatment consisted of two Streptococcus species: S. oralis and S. mitis. After UV irradiation S. vestibularis and S. salivarius were moved into the group of additional microbiota, and N. subflava became part of constant microbiota. The widest diversity of microorganisms was found in the transient microbiota. The average number of microbial species per sample changed from 9±3 (M±SD) in samples without UV treatment to 7±3 (M±SD) in post-UV treatment samples. In the latter, microbiota composition tended to positively change. Treatment of the peri-implantation field with UV leads to lowered peri-implantitis risk, positively affects the pattern of changes in the oral microbiota, leads to reduced isolation of pathogenic microorganisms.
Copyright (c) 2025 Dragunkina O.V., Bochkareva P.V., Bairikov I.M., Samukin A.S., Lyamin A.V., Alekseev D.V. https://creativecommons.org/licenses/by/4.0
Inborn errors of immunity and measles. Case report with fatal outcome
The role of postmortem diagnosis is not only to establish the true cause of death, but also to provide feedback to the physician, the health care system and the patient’s relatives. Identifying the true cause of death can save sibs, future children, and sometimes even the patient’s parents. According to the 2024 classification, there are 555 different forms of inborn errors of immunity, and 17 phenocopies, but many of the patients remain undetected both in life and after death. Inborn errors of immunity (or primary immunodeficiencies) often mimic and hide under the mask of other diseases. Infections in patients with inborn errors of immunity may be atypical, persistently recurrent, and may be life-threatening, leading to death or disability of the patient. The same is true for measles, which in immunodeficient patients of any genesis may develop atypically, often with absent or delayed mucosal and cutaneous rashes, and with typical lung lesions. This article describes a clinical case of pneumonia with probable combined lesions from measles and SARS-CoV-2 viruses complicated by bacterial infection. In this case, an equilibrium translocation of long arm regions between chromosomes 7 and 18 was detected in the patient, his sibs and mother. Although this chromosomal pathology is not listed in the classification of inborn errors of immunity, the list of included diagnoses has been continuously expanding, and the presence of inborn immunodeficiency in this clinical case was confirmed morphologically. The National Association of Experts in Primary Immunodeficiencies has developed warning signs of primary immunodeficiencies that may help in the lifetime diagnosis of these diseases. Neonatal screening for the TREC and KREC markers of lymphopenia helps to identify conditions accompanied by defects in T- and B-lymphocyte maturation, and thymus ultrasound is proved to be an essential diagnostic method that helps to detect changes in thymus (one of the main organs of the immune system) size and structure during life. Morphological study, performed either at lifetime during operative thymus resection or postmortem, allows to reveal characteristic signs of immune system dysembryogenesis, including disturbance of thymus size and histological structure, decrease in the number and changes in the size of Hassall’s corpuscles. Thus, based on clinical, morphological and genetic data it reduces a chance of missing primary immunodeficiency, whereas timely diagnostics opens a window for therapeutic intervention and life-saving.
Copyright (c) 2025 Tuzankina I.A., Bolkov M.A., Krohaleva Y.M., Volodin A.D., Sannikova O.Y., Shinwari K. https://creativecommons.org/licenses/by/4.0
For the anniversary of Vladimir A. Kozlov
Copyright (c) 2025 Editorial T. https://creativecommons.org/licenses/by/4.0