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Other viral infections
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Less is known about neonatal infection with coxsackie A virus. There are case reports of in utero fetal death with disseminated coxsackie A virus. It is rare for coxsackie A virus to be passed to the fetus (42). There appears to be no association between echovirus or coxsackie B virus infection and an increased spontaneous abortion rate. Stillbirth in late pregnancy increases with both maternal echovirus and coxsackie B viral infection. The association between maternal coxsackie B virus infection and a slightly greater risk of fetal urogenital defects and congenital heart defects is tenuous (39,41). Coxsackie B virus, particularly serotypes B3 and B4, has been implicated in neonatal myocarditis (43).
Diagnostic Approach to Fulminant Hepatitis in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Coxsackie B virus (COX B) belongs to a family of RNA viruses, Picornaviridae, that infects the heart, pleura, pancreas, and liver of early infancy, causing pleurodynia, myocarditis, pericarditis, and hepatitis. Coxsackie hepatitis is frequently associated with myocarditis [37]. The ALF develops as part of a disseminated viral infection, where fever, jaundice, and petechiae are the most consistent findings on admission. A biphasic fever pattern has also been reported. Jaundice and coagulopathy are poor prognostic indicators. Laboratory abnormalities include anemia, thrombocytopenia, prolongation of PT and activated thromboplastin time, marked transaminases elevation (AST > ALT), and elevated fibrin degradation product levels [38]. Diagnosis can be made by serological paired complement fixation antibody (IgG and IgM) titers for COX B, with at least a fourfold rise in titer between acute and convalescent phased [37]. The RT-PCR is diagnostic of infection, and cell cultures are useful when isolate serotyping is important. There is no specific therapy for COX B, and treatment includes fluids and supportive care.
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The Epstein-Barr virus is a common cause of hepatitis and is probably related to the development of infectious mononucleosis. In this disease, the liver is involved, with pathologic changes resembling those of infectious hepatitis. Only a few patients develop jaundice or other evidence of severe hepatocellular disease. The biochemical changes are similar to hepatitis A or B and the diagnosis is based on clinical findings which include a characteristic blood picture (monocytosis with aberrant cells), generalized splenomegaly and lymphadenopathy, and positive heterophil antibodies (Paul-Bunnell test). The recovery of Epstein-Barr virus infectious mononucleosis is slow. Herpex simplex virus occasionally produces a highly fatal generalized infection with prominent liver inflammation and necrosis in infants. The Coxsackie B virus group produces hepatitis occasionally.46
Prediction, diagnosis, prevention and treatment: genetic-led care of patients with diabetes
Published in Expert Review of Precision Medicine and Drug Development, 2021
Watip Tangjittipokin, Nutsakol Borrisut, Patcharapong Rujirawan
Not all individuals with high-risk haplotypes develop T1DM. The majority of people with these haplotypes do not. The development of T1DM is likely partly influenced by environmental factors that play a role in triggering autoimmunity. A previous study reported that the development of autoantibodies against islet cells in high-risk individuals often occurs between 9 months to 2 years of age [18]. Viral infection is one of the most studied triggers of T1DM. Many viral infections are associated with T1DM development, including enteroviruses, such as Coxsackie B virus, cytomegalovirus, rubella virus, and rotavirus [19]. The mechanism by which enteroviruses induce autoimmunity remains unclear. However, it was proposed that the enteroviral P2-C protein sequence is similar to glutamic decarboxylase (GAD) in islet cells, and after infection, antibodies can cross-react with islet cells leading to islet cell destruction. Another study proposed that viral induction of T1DM might be due to molecular mimicry [20]. Other factors that continue to be explored are vitamin D deficiency, breastfeeding, milk formula, maternal age, preeclampsia, and childhood obesity.
Role of fever and ambient temperature in COVID-19
Published in Expert Review of Respiratory Medicine, 2021
Muhammad Hamdan Gul, Zin Mar Htun, Asad Inayat
Bats are known to have a vast reservoir of corona-viruses, and COVID-19 is likely to have its origin in bats [9]. During the flight, the bats increase the metabolic rate by 15–16 fold, which is accompanied by high fevers. Daily high temperatures, in the setting of high metabolic rates, attained during the flight activates the immunity and has been proposed as a mechanism through which the bats can harbor pathogenic viruses [10]. The effect of fever or the ambient temperature has been studied previously on other viruses. In the experimental mammalian models, the higher ambient temperature has been shown to enhance resistance against the herpes simplex virus [11]), poliovirus [12], Coxsackie B virus [13], rabies virus [14], influenza virus [15], and gastroenteritis virus [16](Table 1). A population-based study estimated that the use of antipyretic drugs to suppress fever would increase the cases and mortality in influenza [17]. In a randomized controlled trial on 56 volunteers infected with the Rhinovirus, the use of aspirin and acetaminophen was associated with increased nasal symptoms and decreased neutralizing antibody response [18]. In another randomized clinical trial on 72 children, the use of acetaminophen was associated with an increased duration of scabbing in childhood varicella infection [19].
Functional significance of the rare rs35667974 IFIH1 gene polymorphism, associated with multiple autoimmune diseases, using a structural biological approach
Published in Autoimmunity, 2022
Maria I. Zervou, Athena C. Andreou, Elias E. Eliopoulos, George N. Goulielmos
MDA5 was shown to be involved in the modulation of crosstalk between β-cells and the innate/adaptive immune system through the local production of cytokines and chemokines, and changes in MDA5 expression and/or activity may trigger β-cell responses to dsRNA, a by-product of virus replication [8].Therefore, this polymorphism does not affect the nucleotide acid-binding properties of this cytoplasmic RNA sensing helicase but alters its function [25] by a mechanism that is still unknown. An association trend between the IFIH1 I923V variant and frequency of enteroviral RNA in type 1 diabetic patients has also been established [26]. In addition, there is a first report showing a relation between the IFHI1 polymorphism and the incidence of enterovirus infection in T1D. Furthermore, recent studies on MDA5- and MAVS-knockout mice showed a critical role of these proteins in mediating type 1 interferon responses against coxsackie B virus [27]. A mengovirus leader protein is shown to prevent the expression IFN-β by blocking the dimerization of IRF3 needed for the activation of this factor [28]. This observation suggests that IFIH1 variants that disrupt MDA5 function in the host antiviral response have been negatively selected, rather than positively selected because they confer protection from T1D [9]. Identification of shared genetic susceptibility or protection loci may provide insight to our understanding of the pathophysiology of autoimmune diseases. Although the association of rs35667974 variant of IFIH1 locus with multiple autoimmune diseases supports existing evidence for a causal role of the IFIH1 gene in these diseases, further mechanistic studies are needed to confirm that this variant of IFIH1 is indeed causal. Thus, in the framework of the present study we aimed to investigate the potential role of rs35667974 variant, encoding an Ile923Val amino acid change in the IFIH1 gene protein product (MDA5), which is a biologically plausible candidate gene shared by six diseases (including T1D, PS, PsA, AS, CD and UC), from the structural biological point of view. This type of analysis may lead in some cases to a better management of the diseases through the development of shared therapeutic approaches.