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Order Reovirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The Spinareovirinae family also includes a well-known mammalian orthoreovirus type 3 Dearing (MRV-3De) of the Mammalian orthoreovirus species, which attracted special attention as an oncolytic virus and a prospective antitumor agent (for references see Black and Morris 2012). Reolysin® (pelareorep), a clinical formulation of the latter, was evaluated, for example, to treat melanoma (Galanis et al. 2012), head and neck cancer (Kyula et al. 2012), and advanced solid tumors (Morris et al. 2013).
Viruses
Published in Loretta A. Cormier, Pauline E. Jolly, The Primate Zoonoses, 2017
Loretta A. Cormier, Pauline E. Jolly
Other genera of Reoviridae capable of causing symptomatic infection in humans are Orthoreovirus, Orbivirus, Coltivirus, and Seadornavirus (DeBiasi and Tyler 2015). Of these, Orthoreovirus and Orbivirus species have been found in wild primates. Orthoreovirus includes Reovirus types 1, 2, and 3. Infection with Reovirus is common in humans but is typically either asymptomatic or presents as a mild respiratory tract infection or gastrointestinal illness; rarely, it is the causative agent for meningitis, encephalitis, pneumonia, or myocarditis (DeBiasi and Tyler 2015). Few surveys of Reovirus in wild primates have been conducted, but it has been identified in Asian macaques and langurs as well as African baboons. Orbiviruses capable of causing disease in humans include the Kemerovo complex viruses, Lebombo virus, and Changuinola virus (DeBiasi and Tyler 2015). Of these, only the Orungo virus has been found in wild primates. The Orungo virus is a vector-borne parasite that is transmitted by Anopheles, Aedes, and Culex species of mosquitoes (Attoui and Mohd 2015). It is widely distributed in tropical Africa where it has been isolated in monkeys, cattle, camel, sheep, goats as well as humans (Attoui and Mohd 2015). Orungo virus infection is often asymptomatic, but when symptoms occur they include fever, headache, and myalgia with one documented case of it progressing to encephalitis in a child (DeBiasi and Tyler 2015). In humans, seroprevalence rates in some areas of sub-Saharan Africa are between 24% and 35% (DeBiasi and Tyler 2015). A similar rate of 24% has been found in grivets and Mona monkeys in Nigeria (Tomori and Fabiyi 1976), and as such, they should be considered a potential reservoir.
Gut microbiota in Celiac Disease: microbes, metabolites, pathways and therapeutics
Published in Expert Review of Clinical Immunology, 2020
Katherine L Olshan, Maureen M Leonard, Gloria Serena, Ali R Zomorrodi, Alessio Fasano
In considering the gut microbiota, many studies have evaluated pathogenic viruses that cause acute infection and may disrupt the normal balance of the gut microbiota. Several studies have suggested that an increased number of gastrointestinal illnesses during the first 6–18 months of life is associated with an increased risk of CD later in life [76,79,80]. In theory, these infections lead to alterations in the gut microbiota, and contribute to increased intestinal permeability, which may lead to loss of tolerance and onset of CD autoimmunity. Many specific enteric infections such as rotavirus, enterovirus, adenovirus type 12, Orthoreovirus, and Candida albicans have been evaluated [81–85]. Mixed data exists on an association with rotaviruses, which primarily affect the small intestine and were the most common cause of diarrheal infections in infants and young children prior to introduction of a rotavirus vaccine in the early 2000s [86]. A study by Stene et al. found that frequent rotavirus infections were a predictor of a higher risk of CD autoimmunity [87]. However, a recent study reported a 1.5% increase in the prevalence of CD over the past 25 years despite the introduction of the rotavirus vaccine in the intervening time period, which argues against any increased risk [88]. Enteroviruses have also been linked to an increased risk of CD [81]. A prospective cohort study by Lindfors et al. found that between the ages of one and two years old, the cumulative number of enteroviral exposures increased the risk of CD autoimmunity [81]. Adenovirus type 12, which has amino acid sequence homology to a specific gliadin protein, has been shown to have a positive association with the later development of CD in multiple studies [82,83]. Also implicated is Orthoreovirus, a virus that causes both respiratory and gastrointestinal infections and is proposed to stimulate inappropriate immune activation, which subsequently leads to loss of tolerance to gliadin and increased intestinal inflammation and permeability [84]. Finally, C. albicans expresses a hyphal wall protein (hyphal wall protein 1) that is structurally similar to several gliadin epitopes, and has been proposed as a possible trigger for CD [85]. However, despite these associations, no studies evaluating the role of gastrointestinal infection on the microbiota in CD have been completed to date, though studies performed in otherwise healthy children with acute gastroenteritis suggest that these infections may lead to alterations in the microbiota, including alterations in microbial diversity [89,90].