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Amantadine and Rimantadine
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Early studies by Maassab and Cochran (1964) showed high concentrations of amantadine could inhibit rubella in vitro. Sindbis virus was resistant (Cassell et al., 1984), although other investigators reported that Sindbis virus was susceptible to both amantadine and rimantadine (Couch and Howard, 1986). There were conflicting reports regarding the susceptibility of Semliki Forest virus, with documentation of > 90% inhibition by amantadine at high concentration (0.5 mM) (Helenius et al., 1982) as well as full resistance (Couch and Howard, 1986).
Viruses
Published in Loretta A. Cormier, Pauline E. Jolly, The Primate Zoonoses, 2017
Loretta A. Cormier, Pauline E. Jolly
Alphaviruses outside of the Semliki Forest complex that have been detected in both humans and wild primates are eastern equine encephalitis virus (EEEV) and Sindbis virus. EEEV is maintained in an avian/mosquito transmission cycle in North America, South America, and the Caribbean (Markoff 2015). Culiseta species mosquitoes are most important in avian transmission, with Coquillettidia and Aedes species mosquitoes being important bridge vectors to humans, horses, and other mammals (Go et al. 2014). In Bolivia, seropositivity has been identified in Ateles species monkeys in the wild. Wild monkey, like humans and other mammals, appear to be incidentally infected. Sindbis virus belongs to the western equine encephalitis complex and, like EEEV, is maintained in an avian/mosquito transmission cycle (Markoff 2015). Culex, Culiseta, and Aedes mosquito species have been identified as important vectors (Adouchief et al. 2016). Sindbis virus occurs in Eurasia, Oceania, and South Africa (Adouchief et al. 2016). Symptoms are similar to those of the Semliki Forest complex with fever, arthralgia, and rash (Markoff 2015). Among wild primates, seropositivity has been identified in orangutans in Borneo.
Neurological Chikungunya
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Vincent G. Thon-Hon, Shiril Kumar, Duksha Ramful, Stephanie Robin, Marie Christine Jaffar-Bandjee, Philippe Gasque
The alphavirus group comprises 29 viruses, six of which are called Old World alphaviruses, and they can cause human joint disorders (arthralgia evolving to arthritis). This is the case for CHIKV, o’nyong-nyong virus (ONNV), Semliki forest virus (SFV), Ross River (RRV), Sindbis virus (SINV), and Mayaro virus (MAYV). The acute phase of the disease with Old World alphaviruses is highly symptomatic (>90%) and is characterized mostly by fever, generalized myalgia, and arthralgia (Borgherini et al. 2008, 2007). Arthralgia and crippling arthritis are symptoms that can persist for years (Simon et al. 2011; Sissoko et al. 2009).
Merits of the ‘good’ viruses: the potential of virus-based therapeutics
Published in Expert Opinion on Biological Therapy, 2021
Qianyu Zhang, Wen Wu, Jinqiang Zhang, Xuefeng Xia
Virosomes are reconstituted virus-mimicking envelopes composed of membrane lipids and viral spike glycoproteins, along with other synthetic or natural lipid components such as phospholipids. Virosome is a hybrid drug delivery system composed of viral and non-viral vector apparatus, which is developed to combine their advantages. Non-viral vectors are generally safer but less efficient in nucleic acid delivery than their viral counterparts and viral vectors are not as versatile as non-viral vectors in regards to the delivered cargo (such as in the delivery of proteins). Virosome was first prepared by inserting purified influenza spike proteins into preformed phospholipid-based liposomes [86]. Other virosomes have been devised including Sendai virus, Sindbis virus, Semliki Forest virus (SFV), and vesicular stomatitis virus (VSV) [87–90].
The discovery and development of mRNA vaccines for the prevention of SARS-CoV-2 infection
Published in Expert Opinion on Drug Discovery, 2023
Vivian Weiwen Xue, Sze Chuen Cesar Wong, Bo Li, William Chi Shing Cho
The prototype of self-amplifying mRNA (saRNA) vaccines involves integrating viral fragments of interest into RNA viruses that have the reproductive ability to establish a vaccine. This is based on alphaviruses, including the Semliki Forest virus, Sindbis virus, and Venezuelan equine encephalitis virus [48,49]. Except for a 5’ cap and a 3’ poly(A) tail, saRNA has a basic structure that contains four nonstructural genes NSP1–4, 26S subgenomic promoter, and the gene of interest [50]. The NSP1–4 polyprotein serves as a replicase to initially amplify the complete saRNA sequence, after which it is self-cleaved and prioritized to amplify the gene of interest downstream of the 26S subgenomic promoter [51].
Spectrum of candidate molecules against Chikungunya virus - an insight into the antiviral screening platforms
Published in Expert Review of Anti-infective Therapy, 2019
Shree Madhu Bhat, Piya Paul Mudgal, Sudheesh n, Govindakarnavar Arunkumar
In another study, the efficacy of shRNA was tested using cell lines – HeLa, BHK, and RD cells. Cell clones were engineered to express shRNA against the CHIKV nsP1 and E1. Treatment with shRNA significantly inhibited CHIKV production [92]. No inhibition of DENV and Sindbis virus replication indicated high specificity of the shRNA E1 clones against CHIKV replication [92].