Pathogenesis Of Infectious Diseases Research Articles

Human Babesia odocoilei and Bartonella spp. co-infections in the Americas

BackgroundIn recent years, Babesia and Bartonella species co-infections in patients with chronic, nonspecific illnesses have continued to challenge and change the collective medical understanding of “individual pathogen” vector-borne infectious disease dynamics, pathogenesis and epidemiology. The objective of this case series is to provide additional molecular documentation of Babesia odocoilei infection in humans in the Americas and to emphasize the potential for co-infection with a Bartonella species.MethodsThe development of improved and more sensitive molecular diagnostic techniques, as confirmatory methods to assess active infection, has provided increasing clarity to the healthcare community.ResultsUsing a combination of different molecular diagnostic approaches, infection with Babesia odocoilei was confirmed in seven people suffering chronic non-specific symptoms, of whom six were co-infected with one or more Bartonella species.ConclusionsWe conclude that infection with Babesia odocoilei is more frequent than previously documented and can occur in association with co-infection with Bartonella spp.Graphical

Understanding the Pathogenesis of Infectious Diseases: Insights from Pathology

The pathogenesis of infectious diseases is essential for developing effective diagnostic, therapeutic, and preventive measures. Pathology, the study of disease mechanisms through the examination of tissues and organs, provides critical insights into how pathogens cause disease in their hosts. This paper presents a comprehensive framework for understanding the pathogenesis of infectious diseases, focusing on bacterial, viral, fungal, and parasitic infections. We explore the stages of disease development, including pathogen entry, colonization, immune evasion, tissue damage, and transmission. Key pathological techniques such as histopathology, gross pathology, and molecular pathology are discussed, highlighting their role in identifying and characterizing disease mechanisms. Through detailed case studies, we illustrate how pathological findings inform our understanding of specific infectious diseases, including tuberculosis, HIV/AIDS, and malaria. The significance of host factors, such as genetic variability and immune response, in disease pathogenesis is also examined. Furthermore, the paper addresses the therapeutic implications of these insights, including the development of targeted therapies and vaccines. Finally, we discuss future directions in the field, emphasizing the need for interdisciplinary collaboration and technological advancements to enhance our understanding of infectious disease pathogenesis. This paper aims to bridge the gap between basic pathological research and clinical applications, ultimately contributing to improved public health outcomes.

Functional probes for the diagnosis and treatment of infectious diseases

AbstractInfectious diseases present significant challenges to global health, thereby extensively affecting both human society and the economy. In recent years, functional probes have demonstrated remarkable potential as crucial biomedical media for the research and treatment of infectious diseases. Their applications in the realm of infectious diseases include pathogen detection, exploration of biological mechanisms, and development of anti‐infective drugs. This review provides a concise introduction to the severity, classification, and pathogenesis of infectious diseases. Subsequently, we examined the distinctiveness and design strategies of functional probes for diagnosing and treating infectious diseases, shedding light on their design rationale using typical examples. We discuss the current status and challenges associated with the clinical implementation of functional probes. Furthermore, we explored the prospects of using these probes for the diagnosis and treatment of infectious diseases. This review aims to offer novel insights into the design of diagnostic probes for infectious diseases and broaden their applications in disease treatment.

Evaluating the antibody response elicited by diverse HIV envelope immunogens in the African green monkey (Vervet) model

African Green (Vervet) monkeys have been extensively studied to understand the pathogenesis of infectious diseases. Using vervet monkeys as pre-clinical models may be an attractive option for low-resourced areas as they are found abundantly and their maintenance is more cost-effective than bigger primates such as rhesus macaques. We assessed the feasibility of using vervet monkeys as animal models to examine the immunogenicity of HIV envelope trimer immunogens in pre-clinical testing. Three groups of vervet monkeys were subcutaneously immunized with either the BG505 SOSIP.664 trimer, a novel subtype C SOSIP.664 trimer, CAP255, or a combination of BG505, CAP255 and CAP256.SU SOSIP.664 trimers. All groups of vervet monkeys developed robust binding antibodies by the second immunization with the peak antibody response occurring after the third immunization. Similar to binding, antibody dependent cellular phagocytosis was also observed in all the monkeys. While all animals developed potent, heterologous Tier 1 neutralizing antibody responses, autologous neutralization was limited with only half of the animals in each group developing responses to their vaccine-matched pseudovirus. These data suggest that the vervet monkey model may yield distinct antibody responses compared to other models. Further study is required to further determine the utility of this model in HIV immunization studies.

Unlocking the power of Zc3h12c: Orchestrating Macrophage activation and elevating the innate immune response

The activation of macrophages, essential for the innate defense against invading pathogens, revolves around Toll-like receptors (TLRs). Nevertheless, a comprehensive understanding of the molecular mechanisms governing TLR signaling in the course of macrophage activation remains to be fully clarified. Although Zc3h12c was originally identified as being enriched in organs associated with macrophages, its precise function remains elusive. In this study, we observed a significant induction of Zc3h12c in macrophages following stimulation with TLR agonists and pathogens. Overexpression of Zc3h12c significantly mitigated the release of TNF-α and IL-6 triggered by lipopolysaccharide (LPS), whereas depletion of Zc3h12c increased the production of the cytokines mentioned above. Notably, the expression of IFN-β was not influenced by Zc3h12c. Luciferase reporter assays revealed that Zc3h12c could suppress the TNF-α promoter activity. Moreover, Zc3h12c exerted a notable inhibitory effect on JNK, ERK, p38, and NF-κB signaling induced by LPS. In summary, the findings of our study suggest that Zc3h12c functions as a robust suppressor of innate immunity, potentially playing a role in the pathogenesis of infectious diseases.

Neurobrucellosis (Brucella ceti) in striped dolphins (Stenella coeruleoalba): Immunohistochemical studies on immune response and neuroinflammation.

Neurobrucellosis is a shared condition of cetaceans and humans. However, the pathogenesis and immune response in cetacean neurobrucellosis has not been extensively studied. In this multicentric investigation, 21 striped dolphin (Stenella coeruleoalba) neurobrucellosis (Brucella ceti) cases diagnosed over a 10-year period (2012-2022) were retrospectively evaluated. For each case, morphological changes were assessed by evaluating 21 histological parameters. Furthermore, the immunohistochemical expression of Brucella antigen, glial fibrillary acid protein (GFAP), and a selection of inflammatory cell (IBA-1, CD3, and CD20) and cytokine (tumor necrosis factor-alpha [TNF-α], interferon-gamma [IFN-γ], interleukin [IL]-1β, IL-2, and IL-6) markers were investigated. Inflammation of the leptomeninges, ependyma, and/or choroid plexus was lymphohistiocytic, containing macrophages/microglia (IBA-1+), T-cells (CD3+), and B-cells (CD20+) in equal proportion. B-cells occasionally formed tertiary follicles. GFAP expression showed astrocytosis in most cases. Expression of TNF-α, IFN-γ, and IL-2 indicated an intense proinflammatory response, stimulating both macrophages and T-cells. Our results showed that the inflammation and neuroinflammation in neurobrucellosis of striped dolphins mimic human neurobrucellosis and in vitro and in vivo studies in laboratory animals. Cetacean disease surveillance can be exploited to expand the knowledge of the pathogenesis and immunology of infectious diseases, particularly brucellosis, under a One Health approach.

A long journey to the colon: The role of the small intestine microbiota in intestinal disease.

The small intestine represents a complex and understudied gut niche with significant implications for human health. Indeed, many infectious and non-infectious diseases center within the small intestine and present similar clinical manifestations to large intestinal disease, complicating non-invasive diagnosis and treatment. One major neglected aspect of small intestinal diseases is the feedback relationship with the resident collection of commensal organisms, the gut microbiota. Studies focused on microbiota-host interactions in the small intestine in the context of infectious and non-infectious diseases are required to identify potential therapeutic targets dissimilar from those used for large bowel diseases. While sparsely populated, the small intestine represents a stringent commensal bacterial microenvironment the host relies upon for nutrient acquisition and protection against invading pathogens (colonization resistance). Indeed, recent evidence suggests that disruptions to host-microbiota interactions in the small intestine impact enteric bacterial pathogenesis and susceptibility to non-infectious enteric diseases. In this review, we focus on the microbiota's impact on small intestine function and the pathogenesis of infectious and non-infectious diseases of the gastrointestinal (GI) tract. We also discuss gaps in knowledge on the role of commensal microorganisms in proximal GI tract function during health and disease.

Oxidative stress induced by the human microbiota yeast component as a micromycetes pathogenicity factor

The introduction of MALDI-ToF mass spectrometry into routine microbiological diagnostics has led to a widely extended list of identified microorganisms. This phenomenon also affected mycological studies. Rare basidiomycetes and ascomycetes began to be detected in various types of pathological material. It is often difficult to assess a role of isolated micromycetes in the pathogenesis of a certain disease. In addition to generally admitted pathogenicity factors, such as aggression enzymes, adhesive activity, and toxin formation, induction or inhibition of reactive oxygen species can play a prominent role in pathogenesis of infectious diseases. In our study, we evaluated the total prooxidant and total antioxidant activity of cultivated ascomycete and basidiomycete yeasts from the human intestinal mycobiome. The strains of micromycetes assessed here were obtained from a fecal culture study from patients with gastrointestinal tract pathology and healthy people undergoing a routine medical examination. Identification was carried out analyzing morphological, cultural, biochemical properties and confirmed by mass spectrometry. The total prooxidant and antioxidant activity was assessed by the induced or inhibited malondialdehyde formation during Tween-80 oxidation. It was found that the level of total prooxidant activity in Rhodotorula mucilaginosa, Geotrichum candidum, Candida albicans, Pichia kudriavzevii significantly exceeds the level of total antioxidant activity, and the Pichia kudriavzevii prooxidase activity was more than twice as high as in other studied micromycetes. The revealed ability of some fungi to induce oxidase stress can be considered as one of significant pathogenicity factors of microorganisms that cause pathomorphological changes in human intestinal tissues.

Mesenchymal Stem Cell-Derived Exosomes Attenuate Murine Cytomegalovirus-Infected Pneumonia via NF-κB/NLRP3 Signaling Pathway.

Reactivation and infection with cytomegalovirus (CMV) are frequently observed in recipients of solid organ transplants, bone marrow transplants, and individuals with HIV infection. This presents an increasing risk of allograft rejection, opportunistic infection, graft failure, and patient mortality. Among immunocompromised hosts, interstitial pneumonia is the most critical clinical manifestation of CMV infection. Recent studies have demonstrated the potential therapeutic benefits of exosomes derived from mesenchymal stem cells (MSC-exos) in preclinical models of acute lung injury, including pneumonia, ARDS, and sepsis. However, the role of MSC-exos in the pathogenesis of infectious viral diseases, such as CMV pneumonia, remains unclear. In a mouse model of murine CMV-induced pneumonia, we observed that intravenous administration of mouse MSC (mMSC)-exos reduced lung damage, decreased the hyperinflammatory response, and shifted macrophage polarization from the M1 to the M2 phenotype. Treatment with mMSC-exos also significantly reduced the infiltration of inflammatory cells and pulmonary fibrosis. Furthermore, in vitro studies revealed that mMSC-exos reversed the hyperinflammatory phenotype of bone marrow-derived macrophages infected with murine CMV. Mechanistically, mMSC-exos treatment decreased activation of the NF-κB/NLRP3 signaling pathway both in vivo and in vitro. In summary, our findings indicate that mMSC-exo treatment is effective in severe CMV pneumonia by reducing lung inflammation and fibrosis through the NF-κB/NLRP3 signaling pathway, thus providing promising therapeutic potential for clinical CMV infection.

Immunotherapy with genetically engineered T cells holds promise for the treatment of nonmalignant diseases in the dog.

The ability to genetically redirect the antigenic specificity of T cells using chimeric antigen receptors (CAR) has led to unprecedented durable clinical remissions in human patients with relapsed/refractory hematological malignancies. This remarkable advance in successful immune cell engineering has now led to investigations into the application of CAR-T-cell technology to treat nonmalignant diseases. The use of CAR-T cells to target and eliminate specific cell subsets involved in the pathogenesis of autoimmunity, fibrosis, senescence, and infectious disease represents a new direction for adoptive cell therapies. While the use of CAR-T cells for nonmalignant disease is still in its infancy, early reports of dramatic clinical responses to CAR-T cells targeting CD19+ B cells in patients with severe autoimmune disease raise the possibility that this approach could lead to durable remissions, eliminating the need for ongoing conventional immunosuppressive therapies. Excitingly, nonmalignant disease processes that may be addressed by CAR-T-cell therapy in humans also occur in our canine populations. Given that technologies for developing canine CAR constructs are now available, robust protocols have been described for generating canine CAR-T cells, and experience is being gathered with their clinical use in oncology, it is anticipated that CAR-T cells will soon enter the veterinary clinics for the treatment of debilitating nonmalignant diseases. Here, we provide a broad overview of CAR-T-cell therapies for nonmalignant diseases and extrapolate these advances into the veterinary space, highlighting areas in which canine CAR-T cells are poised to enter the clinics for the treatment of nonmalignant disease.

Emerging Role of Mast Cells as Biological Markers in the Pathogenesis of Infectious Diseases and their Projection in Health Emergencies

Emerging Role of Mast Cells as Biological Markers in the Pathogenesis of Infectious Diseases and their Projection in Health Emergencies

Extracellular vesicles and endothelial dysfunction in infectious diseases

AbstractCardiovascular diseases (CVDs) remain the leading cause of mortality and morbidity globally. Studies have shown that infections especially bacteraemia and sepsis are associated with increased risks for endothelial dysfunction and related CVDs including atherosclerosis. Extracellular vesicles (EVs) are small, sealed membrane‐derived structures that are released into body fluids and blood from cells and/or microbes and are critically involved in a variety of important cell functions and disease development, including intercellular communications, immune responses and inflammation. It is known that EVs‐mediated mechanism(s) is important in the development of endothelial dysfunction in infections with a diverse spectrum of microorganisms including Escherichia coli, Candida albicans, SARS‐CoV‐2 (the virus for COVID‐19) and Helicobacter pylori. H. pylori infection is one of the most common infections globally. During H. pylori infection, EVs can carry H. pylori components, such as lipopolysaccharide, cytotoxin‐associated gene A, or vacuolating cytotoxin A, and transfer these substances into endothelial cells, triggering inflammatory responses and endothelial dysfunction. This review is to illustrate the important role of EVs in the pathogenesis of infectious diseases, and the development of endothelial dysfunction in infectious diseases especially H. pylori infection, and to discuss the potential mechanisms and clinical implications.

Intracellular Staphylococcus aureus infection in human osteoblasts: circRNA expression analysis

Staphylococcus aureus (S. aureus) has the ability to invade human cortical bones and cause intracellular infections in osteoblasts, which may lead to a long-term infection that is difficult to eliminate. It is critical to identify the underlying mechanisms of the osteoblast response to the intracellular S. aureus. More recently, multiple circular RNA (circRNA) functions have been identified, including serving as protein scaffolds or miRNA sponges and being translated into polypeptides. The role that circRNAs play in intracellular S. aureus infection of osteoblasts has not, to our knowledge, been investigated. Here, we established an intracellular infection model of S. aureus in osteoblasts and compared the circRNA expression of osteoblasts between the infected and control groups using RNA sequencing technology, by which a significant difference was found. In total, 117 upregulated and 125 down-regulated differentially expressed circRNAs (DEcircRNAs) were identified, and reverse transcription-quantitative PCR was employed to validate the results of RNA sequencing. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses demonstrated that DEcircRNAs were enriched in processes associated with macromolecule modification, cellular component organization or biogenesis, and intracellular non-membrane-bound organelles. Finally, a potentially important network of circRNA-miRNA-mRNA based on the DEcircRNAs was constructed. Overall, this study revealed the circRNA expression profile of human osteoblasts infected by intracellular S. aureus for the first time, and identified the circRNAs that may contribute to the pathogenesis of infectious diseases caused by intracellular S. aureus infection in human osteoblasts.

Lipid Nanocarriers-Enabled Delivery of Antibiotics and Antimicrobial Adjuvants to Overcome Bacterial Biofilms.

The opportunistic bacteria growing in biofilms play a decisive role in the pathogenesis of chronic infectious diseases. Biofilm-dwelling bacteria behave differently than planktonic bacteria and are likely to increase resistance and tolerance to antimicrobial therapeutics. Antimicrobial adjuvants have emerged as a promising strategy to combat antimicrobial resistance (AMR) and restore the efficacy of existing antibiotics. A combination of antibiotics and potential antimicrobial adjuvants, (e.g., extracellular polymeric substance (EPS)-degrading enzymes and quorum sensing inhibitors (QSI) can improve the effects of antibiotics and potentially reduce bacterial resistance). In addition, encapsulation of antimicrobials within nanoparticulate systems can improve their stability and their delivery into biofilms. Lipid nanocarriers (LNCs) have been established as having the potential to improve the efficacy of existing antibiotics in combination with antimicrobial adjuvants. Among them, liquid crystal nanoparticles (LCNPs), liposomes, solid lipid nanoparticles (SLNs), and nanostructured lipid carriers (NLCs) are promising due to their superior properties compared to traditional formulations, including their greater biocompatibility, higher drug loading capacity, drug protection from chemical or enzymatic degradation, controlled drug release, targeted delivery, ease of preparation, and scale-up feasibility. This article reviews the recent advances in developing various LNCs to co-deliver some well-studied antimicrobial adjuvants combined with antibiotics from different classes. The efficacy of various combination treatments is compared against bacterial biofilms, and synergistic therapeutics that deserve further investigation are also highlighted. This review identifies promising LNCs for the delivery of combination therapies that are in recent development. It discusses how LNC-enabled co-delivery of antibiotics and adjuvants can advance current clinical antimicrobial treatments, leading to innovative products, enabling the reuse of antibiotics, and providing opportunities for saving millions of lives from bacterial infections.

Type I Interferon Signalling and Ischemic Stroke: Mechanisms and Therapeutic Potentials.

Type I interferon (IFN-I) signalling is intricately involved in the pathogenesis of multiple infectious diseases, autoimmune diseases, and neurological diseases. Acute ischemic stroke provokes overactivation of IFN-I signalling within the injured brain, particularly in microglia. Following cerebral ischemia, damage-associated molecular patterns (DAMPs) released from injured neural cells elicit marked proinflammatory episodes within minutes. Among these, self-nucleic acids, including nuclear DNA and mitochondrial DNA (mtDNA), have been recognized as a critical alarm signal to fan the flames of neuroinflammation, predominantly via inducing IFN-I signalling activation in microglia. The concept of interferon-responsive microglia (IRM), marked by upregulation of a plethora of IFN-stimulated genes, has been emergingly elucidated in ischemic mouse brains, particularly in aged ones. Among the pattern recognition receptors responsible for IFN-I induction, cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) plays integral roles in potentiating microglia-driven neuroinflammation and secondary brain injury after cerebral ischemia. Here, we aim to provide an up-to-date review on the multifaceted roles of IFN-I signalling, the detailed molecular and cellular mechanisms leading to and resulting from aberrant IFN-I signalling activation after cerebral ischemia, and the therapeutic potentials. A thorough exploration of these above points will inform our quest for IFN-based therapies as effective immunomodulatory therapeutics to complement the limited repertoire of thrombolytic agents, thereby facilitating the translation from bench to bedside.

Characteristics of Bacterial Biofilm Formation in Nasolacrimal Silicone Tubes Post-dacryocystorhinostomy.

To examine the biofilm formation characteristics of bacteria identified at the genus level in samples obtained from silicone tubes after dacryocystorhinostomy surgery. In the study involving consecutive patients who underwent dacryocystorhinostomy surgery at Ankara Bilkent City Hospital and whose silicone tubes were removed six months after surgery, between January 2023 and May 2023; the tubes were placed in glycerol-PBS (phosphate buffered saline) solution and cultured on descriptive selective media at the genus level. The biofilm-forming properties of the obtained isolates were examined in solid-air and liquid-air interphases. Salmonella Typhimurium ATCC SL1344 strain was used as the control bacterium. As a result of the analysis of the samples taken from the patients, Pseudomonas spp. was identified in three of the samples, Staphylococcus spp. in five of the samples, and Streptococcus spp. in one of the samples. Among these samples, except for the bacteria identified in samples one and five, the rest were found to be strong biofilm producers. In all strong biofilm producers, the maximum biofilm production time was determined as 72 h and the incubation temperature was 37°C. The presence of cellulose and amyloid proteins in biofilm matrix structures is identified. Swimming and swarming motilities were observed in all bacterial samples. Since biofilms are considered potential factors in the pathogenesis of infectious and inflammatory diseases, they are a subject that needs to be thoroughly investigated. In our study, although there were no clinical infections in any of the patients, biofilm formation was detected in the patient samples. The fact that the bacteria exhibited moderate to strong biofilm formation characteristics suggests that these microorganisms could be persistent infectious agents.

Ferritinophagy: A novel insight into the double-edged sword in ferritinophagy-ferroptosis axis and human diseases.

Nuclear receptor coactive 4 (NCOA4), which functions as a selective cargo receptor, is a critical regulator of the particularly autophagic degradation of ferritin, a process known as ferritinophagy. Mechanistically, NCOA4-mediated ferritinophagy performs an increasingly vital role in the maintenance of intracellular iron homeostasis by promoting ferritin transport and iron release as needed. Ferritinophagy is not only involved in iron-dependent responses but also in the pathogenesis and progression of various human diseases, including metabolism-related, neurodegenerative, cardiovascular and infectious diseases. Therefore, ferritinophagy is of great importance in maintaining cell viability and function and represents a potential therapeutic target. Recent studies indicated that ferritinophagy regulates the signalling pathway associated with ferroptosis, a newly discovered type of cell death characterised by iron-dependent lipid peroxidation. Although accumulating evidence clearly demonstrates the importance of the interplay between dysfunction in iron metabolism and ferroptosis, a deeper understanding of the double-edged sword effect of ferritinophagy in ferroptosis has remained elusive. Details of the mechanisms underlying the ferritinophagy-ferroptosis axis in regulating relevant human diseases remain to be elucidated. In this review, we discuss the latest research findings regarding the mechanisms that regulate the biological function of NCOA4-mediated ferritinophagy and its contribution to the pathophysiology of ferroptosis. The important role of the ferritinophagy-ferroptosis axis in human diseases will be discussed in detail, highlighting the great potential of targeting ferritinophagy in the treatment of diseases.

The Gain-of-Function Research in Virology: Concerns, Risks, and Benefits

Gain-of-function (GOF) research is biotechnological research that genetically modifies microbial gene products to enhance their biological function. The basic aim of this research is to elucidate the pathogenesis of infectious diseases, develop new vaccines and therapeutics, improve cancer treatments, and achieve specific goals by adding beneficial trait expression to the genome. Despite these significant potential benefits, GOF research can pose some important and serious biosafety risks. The main group of pathogens of concern in GOF research are respiratory viruses with pandemic potential. While laboratory accidents and ongoing discussions in recent years have raised important awareness that these studies should be carried out in high-safety laboratories, concerns about the results of these studies remain unclear due to the inadequacy or absence of mechanisms to prevent misuse for informal research, despite the strict controls in research funded by international organizations. The most important issue to be discussed is the need to establish regulations that ensure the sustainability of scientific studies and developments that can benefit humanity, as well as strict control or, if necessary, a moratorium on potentially risky research. Debates on the value, safety, ethics, and validity of GOF studies are still ongoing. In this article, it is aimed to examine the status of GOF research in virology, with examples from the current literature, together with benefit and risk perspectives.

The Impact and Effects of Host Immunogenetics on Infectious Disease Studies Using Non-Human Primates in Biomedical Research.

Understanding infectious disease pathogenesis and evaluating novel candidate treatment interventions for human use frequently requires prior or parallel analysis in animal model systems. While rodent species are frequently applied in such studies, there are situations where non-human primate (NHP) species are advantageous or required. These include studies of animals that are anatomically more akin to humans, where there is a need to interrogate the complexity of more advanced biological systems or simply reflect susceptibility to a specific infectious agent. The contribution of different arms of the immune response may be addressed in a variety of NHP species or subspecies in specific physiological compartments. Such studies provide insights into immune repertoires not always possible from human studies. However, genetic variation in outbred NHP models may confound, or significantly impact the outcome of a particular study. Thus, host factors need to be considered when undertaking such studies. Considerable knowledge of the impact of host immunogenetics on infection dynamics was elucidated from HIV/SIV research. NHP models are now important for studies of emerging infections. They have contributed to delineating the pathogenesis of SARS-CoV-2/COVID-19, which identified differences in outcomes attributable to the selected NHP host. Moreover, their use was crucial in evaluating the immunogenicity and efficacy of vaccines against COVID-19 and establishing putative correlates of vaccine protection. More broadly, neglected or highly pathogenic emerging or re-emergent viruses may be studied in selected NHPs. These studies characterise protective immune responses following infection or the administration of candidate immunogens which may be central to the accelerated licensing of new vaccines. Here, we review selected aspects of host immunogenetics, specifically MHC background and TRIM5 polymorphism as exemplars of adaptive and innate immunity, in commonly used Old and New World host species. Understanding this variation within and between NHP species will ensure that this valuable laboratory source is used most effectively to combat established and emerging virus infections and improve human health worldwide.

To the history of pandemics: statistics and forecast.

The article is devoted to the study of human experience related to fight against a viral disease known as influenza infection. The outbreaks of the disease occurred over several millennia and described in the surviving documentary sources are considered. The main attention is paid to investigations of native epidemiologists on this problem. In particular, an analysis of works published more than 80 years ago is shown. It is emphasized that some elements of the influenza epidemic described in this publication are in many respects similar to the features of the modern coronavirus pandemic. History of studies devoted to mechanism of infection transmission is described. Significant attention is paid to the developments of scientists associated with the problem of identifying the causative agent of the disease. The contribution of native scientists in revealing the features of the pathogenesis of infection diseases is highlighted. It is noted that important factors in the spread of infection nowadays are globalization and migration processes. It is emphasized that the speed of infectious diseases spread is considerably caused by the capabilities of modern transport too. The history of studies related to the prevention of influenza by immunization and vaccination is reviewed. A comparative analysis of the application of these prophylactic arrangements in a historical retrospective is given. The possibility of preventing the spread of a viral infection by taking appropriate measures was emphasized. The important role of the mass media is indicated, which consists in timely and truthful information of the population. The position of leading modern scientists on this issue, in particular, M. Honigsbaum, K. G. Vasiliev, S. V. Komisarenko etc. is cited. It is summarized, that the works of native epidemiologists L. V. Hromashevskyi, N. F. Gamaleya, D. S. Samoilovych and others has not lost its relevance and can be the basis for the searching effective methods to combat influenza infection in future.