China
Africa
Explore chapters and articles related to this topic
Mosquitoes
Published in Jerome Goddard, Public Health Entomology, 2022
Ross River virus disease. Ross River (RR) disease, also called epidemic polyarthritis, occurs throughout most of Australia and occasionally New Guinea, Fiji, Tonga, and the Cook Islands. It causes fever, headache, fatigue, rash, and—most notably—arthritis in the wrist, knees, ankles, and small joints of the extremities. The disease is not fatal but may be debilitating, with symptoms occurring for weeks or months. RR disease is the most common arboviral disease in Australia with more than 5,000 cases annually.22 During 1997, there were 6,683 cases reported.23 Peak incidence occurs from January through March, when mosquito vectors are most abundant. Research has indicated that most likely kangaroos and wallabies are natural hosts for RR virus. There are several mosquito vectors of RR virus in Australia, but particularly Culex annulirostris inland and Aedes vigilax and Ae. camptorhynchus in northern and southern coastal areas, respectively.
The Aedes Fauna: Different Aedes Species Inhabiting the Earth
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Annette Angel, Bennet Angel, Neelam Yadav, Jagriti Narang, Surender Singh Yadav, Vinod Joshi
The species is known to be the vector for Wucheria bancrofti and thus responsible for transmitting lymphatic filariasis (Belkin, 1962; Samarawickrema et al., 1993). Dengue virus has also been transmitted by Aedes polynesiensis (Maguire et al., 1971; Rosen et al., 1985; Russell et al., 2005). In vitro studies performed have also shown the species to transmit Murray Valley encephalitis, chikungunya virus, and Ross river virus (Gilotra and Shah, 1967; Gubler, 1981; Kessel, 1971; Maguire et al., 1971; Richard et al., 2016; Rosen, 1955).
Multiple Sclerosis
Published in Irun R. Cohen, Perspectives on Autoimmunity, 2020
Of the virus models, those involving persisting infection, usually with little inflammation in chronic lesions, are regarded as tangential to the MS question and are mentioned only briefly here. On the other hand, viruses which produce chronic inflammatory demyelinative lesions of CNS white matter, whatever their initial target, appear to do so by inducing autoimmunization and, therefore, a form of REAE.63 From the research standpoint, their greatest interest concerns the question how virus infection induces autoimmunization and whether virus persistence is somehow essential to the ongoing process. Models which combine virus infection with purposeful autoimmunization provide an insight into the separate question of vascular events associated with virus infection and the initiation of autoimmune lesions in the CNS. Some of the viruses listed in Table 12 may be incorrectly assigned. It is not clear, for example, where Ross River virus belongs. On the other hand, JHM virus clearly plays both viral roles, persistent infection without inflammation in mice and persistent infection with autoimmunization in rats.
Understanding host responses to equine encephalitis virus infection: implications for therapeutic development
Published in Expert Review of Anti-infective Therapy, 2022
Kylene Kehn-Hall, Steven B. Bradfute
There is little known about host factors needed for subgenomic RNA translation. However, a recent study found that Src kinase facilitates subgenomic RNA translation [89]. Inhibitors of Src family kinases, namely Torin 1 and Dasatinib, decreased CHIKV infectious titers and reduced CHIKV and VEEV structural protein synthesis, with no impact on viral RNA levels. Torin 1 and Dasatinib treatment had a broad impact on alphaviruses, reducing production of CHIKV, VEEV, o’nyong’nyong virus (ONNV), Ross River virus (RRV), and MAYV. Sorafenib, traditionally defined as a Raf kinase inhibitor, was also found to inhibit VEEV production through inhibition of subgenomic protein translation [90]. However, sorafenib’s activity was not dependent on c-Raf and b-Raf, but rather on its suppression of phosphorylation of multiple translational proteins, including eukaryotic initiation factor 4E (eIF4E), 70-kDa ribosomal protein S6 kinase (p70S6K), and ribosomal S6. siRNA studies confirmed the importance of the cap-binding protein eIF4E for VEEV replication. Sorafenib had broad alphavirus activity inhibiting replication of VEEV, EEEV, SINV, and CHIKV.
Is post-COVID syndrome an autoimmune disease?
Published in Expert Review of Clinical Immunology, 2022
Juan-Manuel Anaya, María Herrán, Santiago Beltrán, Manuel Rojas
Over the years, different health crises have arisen caused by viruses or bacteria, such as the Spanish flu, polio, and Ebola. Strikingly, some of the affected patients developed symptoms after the resolution of the disease, as in the case of Spanish influenza, where cases of encephalitis lethargica were reported. Polio also caused a post-polio syndrome [44], and the emergence of autoimmunity has been described in Ebola virus disease survivors [45]. Other examples are Epstein-Barr virus (EBV – glandular fever) and Ross River virus (epidemic polyarthritis), which are commonly associated with long-lasting disabling symptomatology [46,47]. Fatigue, musculoskeletal pain, neurocognitive compromise, and mood disturbances are the most common clinical manifestations after acute disease [47]. Such clinical features may last about six months and may be associated with the acute infection’s severity [47].
Insight into the dichotomous regulation of STING activation in immunotherapy
Published in Immunopharmacology and Immunotoxicology, 2021
Zhaoxue Hu, Yifei Yang, Lincheng Fang, Jinpei Zhou, Huibin Zhang
STING can defend against pathogen invasion through IFN-I, extensive proinflammatory factors, and chemokines, and has a defensive effect against a variety of DNA viruses [105], including hepatitis B virus (HBV), human papillomavirus (HPV), nasopharyngeal cancer-associated EB virus (NPC), and so on [106–109]. In addition, the activation of STING is capable of inhibiting the replication of virus. For instance, DMXAA could inhibit HBV replication in hepatocytes and induce sufficient host immune response to eliminate virus [110]. Gall et al. screened out a novel antiviral small molecule n-(methylcarbamoyl)-2-2-phenylacetamide (C11) through high-throughput screening, which induced interferon secretion in a STING-dependent manner. Treatment with C11 helped produced a cellular status that potentially prevented the replication of various novel emerging types of virus, such as chikungunya virus, Ross River virus, Venezuelan equine encephalitis virus, Mayaro virus, and O'nyong-nyong virus [111].