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At least 19 recordsLinked to original sources
PubMed2026

Dynamic metabolic modelling of ATP allocation during viral infection.

Viral pathogens, like SARS-CoV-2, hijack the host's macromolecular production machinery, imposing an energetic burden that is distributed across cellular metabolism. To explore the dynamic metabolic tension between the host's survival and viral replication, we developed a computational framework that uses genome-scale models to perform dynamic flux balance analysis of human cell metabolism during virus infections. Relative to previous models, our framework addresses the physiology of viral infections of non-proliferating host cells through two new features. First, by incorporating the lipid content of SARS-CoV-2 biomass, we discovered activation of previously overlooked pathways giving rise to new predictions of possible drug targets. Furthermore, we introduce a dynamic model that simulates the partitioning of resources between the virus and the host cell, capturing the extent to which the competition depletes the human cells from essential ATP. By incorporating viral dynamics into our COMETS framework for spatio-temporal modelling of metabolism, we provide a mechanistic, dynamic and generalizable starting point for bridging systems biology modelling with viral pathogenesis. This framework could be extended to broadly incorporate phage dynamics in microbial systems and ecosystems.

Humans↗
PubMed1976

Measurements of the prevalence of viral infections.

Viral diseases exert their major impact through morbidity, impairment of personal health, loss of time at work and school, and cost of medical care. Relatively few of the known viruses cause a significant number of deaths; influenza, childhood viral pneumonia, and hepatitis are the only viral diseases causing more than 1,000 deaths per year. Data based on the National Health Interview Survey of the National Center for Health Statistics show that the common cold annually causes 35.6 acute illnesses per 100 persons. The data reported by the National Therapeutic Disease Index (on the basis of visits by patients to a sample of 1,500 private physicians) show that influenza and other acute respiratory conditions account for about one-third of all visits to physicians. Nearly all viruses first infect humans in infancy and childhood, with a relatively low fatality rate but with frequent episodes of illness.

Adenoviridae↗
PubMed1979

Clinical significance of pulmonary function tests. Alterations in pulmonary function following respiratory viral infection.

Respiratory viral illness is a major cause of morbidity in both adults and children. This report focuses on both the acute and chronic effects on respiratory function of these ubiquitous infections. Infant airways are particularly vulnerable due to the relatively low conductance in immature peripheral airways. Bronchiolitis, caused predominantly by respiratory syncytial virus, is the most important of these viral illnesses and is emerging as a major risk factor for the subsequent development of obstructive airway diseases in adults, possibly by interference with normal alveolar proliferation. The basic pathogenic mechanism involved in adult respiratory viral infection is bronchial hyperreactivity, presumably secondary to epithelial damage and resultant sensitization of rapidly adapting airway receptors. In addition, there may be virus-related alterations in the autonomic and humoral regulation of airway tone. Viral infections may alter the effects of common air pollutants on respiratory function.

Adult↗
PubMed1978

Viral infections.

In summary, viral infections of the skin that occur at adolescence include those typical of childhood and those associated with sexual maturity. Herpes simplex Type II, molluscum contagiosum, and venereal warts, diseases that have shown a marked increase, are in the latter group. Certain diseases, such as rubella, herpes simplex, varicella, and condylomata acuminata, which may lead to laryngeal papillomas, are particularly important because of their effects on the newborn infant. The epidemiological pattern of viral infections changes, and new viruses gain prominence while others fade in importance as causes of disease. Because of this, we can expect new viral entities and changes in earlier ones.

Adolescent↗
PubMed2025

Helminth infections affect host immune responses to viral infections and vaccines.

Helminths are highly prevalent in many regions of the world. Due to the chronic nature of most helminth infections, these parasites are proficient immunomodulators of their hosts. This modulation often leads to skewed or even impaired immune responses against unrelated antigens, such as viruses and vaccines, which can be both beneficial and detrimental for the host. The extent of these effects and the impact on the outcomes of viral infection depends on a variety of factors including timing and tropism of both infections, pathological mechanisms, genetic background, and environmental factors. In this review, we dissect these complex interactions between virus and helminths in the context of coinfection and the impact of helminth infection on antiviral vaccine efficacy. We characterize the key contributing mechanisms that have been defined in preclinical models and human trials and describe the immune actors involved in the modulation of the antiviral and vaccine immune response by helminths. Finally, we address the limitations of our current understanding of helminth-virus interactions.

Helminthiasis↗
PubMed1978

Arthralgias and arthritis in viral infections.

Arthritis and arthralgias are common in many viral infections. They are particularly prominent with hepatitis B virus and rubella infection, where they may be the major presenting symptom. "Lyme arthritis" is also associated with a virus. Similar symptoms are occasionally seen with adenovirus, Coxsackie and echovirus infection. Joint lesions are due to the deposition of immune complexes and not direct viral infection. While the arthritis is usually transient and self-limited, the physician must consider viral infections as etiologic agents of arthralgias and arthritis.

Adult↗
PubMed1978

Countercurrent immunoelectrophoresis in the diagnosis of viral infections of the central nervous system.

Countercurrent immunoelectrophoresis was utilized in the study of 621 specimens of cerebrospinal fluid to determine the correlation of detection of viral antigens with the clinical diagnosis of aseptic meningitis and related viral infections. A panel of viral antisera was immunoelectrophoresed against 119 specimens from patients with suspected viral infections of the central nervous system (group I), 32 from patients with bacterial meningitis (group 2), and 470 from patients with no suspected infection of the nervous system (group 3). One or more precipitin bands were detected in 79% of specimens from group 1, 19% from group 2, and 4% from group 3. Paired acute- and convalescent-phase sera from 32 (78%) of 41 patients with precipitin bands detected by countercurrent immunoelectrophoresis demonstrated a fourfold or greater change in complement-fixing antibodies to the detected antigen. With refinements in antisera, countercurrent immunoelectrophoresis may become useful in the rapid laboratory diagnosis of viral infection of the central nervous system.

Acute Disease↗
PubMed1977

Viral infections in renal transplant donors and their recipients: a prospective study.

The majority of renal allograft recipients develop viral infections, usually with cytomegalovirus (CMV). Their source if virus has not been defined clearly; one possibility if the transplanted kidney itself. To explore this, prospective viral studies were performed on 28 living related donor-recipient pairs. Donors did not have clinical illnesses and viruses were not recovered from throat, urine, or renal tissue, but five (18%) had fourfold rises in antibody titers to herpes group viruses. During the 6 months after transplantation, 24 recipients (86%) had viral infections, 18 of which were associated with CMV. There was no correlation between specific titer rises in the donors and infections in the recipients. Recipients with dual viral infections had more severe clinical courses than those with single infections or with no infection. Recipients with complement-fixing (CF) antibodies to CMV pretransplant had a higher incidence of CMV infections than recipients without pretransplant antibody. Three of seven recipients who lacked CF antibody to CMV and whose donors were seropositive developed clinical illnesses associated with CMV. Latent virus might have been transmitted with the transplanted kidney in these instances, but since lack of CF antibody does not rule out previous CMV infection, the CMV could have been of recipient origin. We conclude that the donor organ is a source of virus for few renal transplant recipients.

Adolescent↗
PubMed1975

Immunopathology of mouse hepatitis virus type 3 infection. III. Clinical and virologic observation of a persistent viral infection.

Three types of viral sensitivity were observed in various mouse strains upon MHV3 infection: resistance, full susceptibility, and semisusceptibility. In the latter type, seen in several inbred strains including C3H, approximately 50% of the adult injected animals resisted to the acute disease. Most of the surviving mice, however, developed a chronic disease with a wasting syndrome and occurrence of paralysis. The chronic period of the disease was characterized by a persistent viral infection, since MHV3 virus was recovered from brain, liver, spleen, and lymph nodes throughout the evolution in most of the animals. In addition, a correlation was observed between the clinical evolution and the titer of virus tested 4 days after infection.

Age Factors↗
PubMed1976

Viral infections that affect the fetus.

Several viral infections besides rubella are known to cause fetal anomalies and disease. Cytomegalovirus, for example, may adversely affect the fetus in a number of ways. Either herpesvirus or hepatitis B virus is transmissible from mother to offspring. Viruses whose potential for fetal harm is less clear are those of varicella, mumps, and influenza.

Congenital Abnormalities↗
PubMed1978

Pituitary-testicular interrelationships in mumps orchitis and other viral infections.

Leydig-cell function was assessed in 27 men with acute mumps orchitis by measuring plasma testosterone concentrations before and after the administration of human chorionic gonadotrophin (HCG). The test was also performed on groups of patients with other febrile viral infections and mumps without orchitis and on healthy euspermic men. The concentrations both before and after HCG were significantly lower in patients in the acute phase of mumps-but not in those with other viral infections and mumps without orchitis-than in the healthy men. Basal concentrations of follicle-stimulating hormone (FSH) and luteinising hormone (LH) were significantly increased in patients with acute mumps orchitis, while an exaggerated response to LH-releasing hormone was noted in four patients after the acute phase of the disease. Raised plasma LH concentrations were also found in several patients with viral infections, including mumps without orchitis. There appeared to be no particular merit of any of the treatments used (aspirin, prednisolone, and cold baths). In patients reevaluated three to five and 10 to 12 months after the acute phase of their disease the basal testosterone concentrations were similar to those of the healthy men, but several of the patients showed a severely impaired response to HCG. Mean basal FSH and LH concentrations were significantly increased 10 to 12 months after the acute phase, while the mean LH concentration was also raised at three to five months.It is concluded that mumps orchitis impairs Leydigcell function during the acute phase of the disease but may also have a more permanent damaging effect, similar to that found in the germinal epithelium.

Acute Disease↗
PubMed2026

Affinity-matured B cell responses neutralizing type-I interferons underlie severe viral infections.

Autoantibodies neutralizing type-I interferons (AAN-I-IFNs) emerge as global, common, and strong determinants of a growing number of severe viral diseases. We report that AAN-I-IFNs+ patients with life-threatening COVID-19 pneumonia harbor circulating type-I IFN-specific B cells indistinguishable from patients bearing T cell tolerance defects of genetic origin. This autoimmune response mobilizes a highly diverse and stable circulating B cell response that is detected prior to severe viral infection and acquires high affinity and neutralization potential to type-I IFNs through extended somatic hypermutation. X-ray crystallography and AlphaFold3 structural analysis of hundreds of patient-derived monoclonal antibodies reveals the extended breadth of this response, targeting three major B cell epitopes covering all facets of type-I IFNs. These findings support a model in which a germinal-center-derived memory B cell response directed against type-I IFNs is established before severe viral infection, providing a core mechanism linking T cell tolerance defect to pathogenic AAN-I-IFNs underlying severe viral diseases.

Humans↗
PubMed1979

[Viral infection and sudden perceptive deafness (serological examinations) (author's transl)].

Among the numerous and various known etiologies of sudden deafness viral infection is discussed. Therefore sera of 126 patients were examined for viral antibodies to Influenza, Parainfluenza, Mumps, Measles, RS-virus, Rubella, Herpesvirus and Adenovirus. They were compared to sera of healthy patients. Our results suggest no strong association between sudden deafness and viral infection.

Adenovirus Infections, Human↗
PubMed1976

Experimental viral infections of the inner ear. I. Acute infections of the newborn hamster labyrinth.

Acute viral infections of the inner ear were produced in neonatal hamsters. Viruses were inoculated percutaneously through the temporal cartilage into the endolymphatic and perilymphatic spaces of the labyrinth or were inoculated intracerebrally to reach the perilymphatic spaces via the cochlear aqueduct. Selective vulnerability of inner ear structures was demonstrated using a variety of viruses. Influenza virus infected only the mesenchymal cells of the perilymphatic channels of the cochlea; mumps virus infected principally endolymphatic structures; herpes simplex virus infected primarily the sensory cells of the labyrinth; and rubeola and vaccinia viruses infected both perilymphatic and endolymphatic cells.

Acute Disease↗
PubMed1975

Immune deficiency in congenital rubella and other viral infections.

No immunologic explanation has been found for the chronicity commonly observed in congenital viral infections. In the presence of a humoral immune response, there is continued viral excretion--in rubella for many months, and in the herpes viruses perhaps for life. Infection with rubella early in utero has a profound effect on the developing immune system. Defects observed are: complete immune paralysis, PHA unresponsiveness, immunoglobulin abnormalities, and loss of antibody to rubella. These defects are transient; absence of IgA may be permanent. No such defects have been observed in other congenital viral infections, but precocious development of immune globulin levels and germinal follicles occurs.

Antibodies, Viral↗
PubMed1979

Neutrophil function in children with acute lymphoblastic leukaemia in the presence and absence of viral infections.

Neutrophil function was assessed regularly in 26 children with acute lymphoblastic leukaemia (ALL) in remission, both when they were well and during viral infections. Tests of candidacidal ability when these children were apparently free of infection showed a trend towards lower levels compared with controls. The most pronounced depression of candidacidal ability and chemotaxis was during viral infections, and these two functions of neutrophils were more likely to be abnormal then than when the children were free of infection. In children with ALL in remission, whose neutrophils may function abnormally even when they are well, the risk of acquiring bacterial or fungal infections may be made greater by virus infections.

Candida albicans↗