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The Viruses
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
A variety of strategies are used to produce attenuated vaccines including adaptation to unnatural host species by serial passage in unnatural host animals or by serial passage in cell culture. Inactivated vaccines are made of whole virus or components of virulent viruses that have been physically or chemically modified to destroy infectivity. They are generally safe and provide protection, but often provide a shorter-lived immunity than do live attenuated vaccines. Commonly used agents to inactivate viruses in the preparation of a “killed” vaccine include formaldehyde, (β-propiolactone, and ethyleneimine.
Order Articulavirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
These live virus strains are cold adapted, temperature sensitive, and attenuated so as not to produce influenza-like illness by limiting their replication to only the upper respiratory tract in humans. The reassortant strains developed by serial passage at sequentially lower temperatures acquire attenuated phenotypes because of multiple mutations in gene segments that encode viral internal proteins (Murphy and Coelingh 2002).
Yellow Fever: Emergence and Reality
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Neelam Yadav, Bennet Angel, Jagriti Narang, Surender Singh Yadav, Vinod Joshi, Annette Angel
The prevalence of YF relies on the transmission by mosquito vector. Hence, it is confined to African and South American tropical countries. However, YF has not been reported in Asia; yet the vector for transmission of YF, that is, A. aegypti, is present in these regions (Barrett and Monath, 2003; Barrett and Higgs, 2007; Gould et al., 2008). Nina et al. (2013) and Stokes et al. (1928) discovered that rhesus monkeys were prone to YFV infection. Bearcroft (1957) demonstrated the pathology of YFV in several organs of Macaca mulatta. Theiler (1936) showed the similarity of YF pathology between monkey and human. Tigertt et al. (1960) comprehensively studied the pathology of YF in the liver of M. mulatta.Lloyd et al. (1936) demonstrated that the Asibi strain of YFV lost its virulence during continuous passage in cell culture. Hardy (1963) and Hearn et al. (1966) reported viral virulence during serial passage in animal cell cultures. This was because of differences in the rates of virus attenuation upon passage of many cell lines, which may reflect the nutritional or metabolic differences of culturing cells. John et al. (1971) studied the altered virulence pattern of YFV by using cell lines and comparative pathology of passaged and unpassaged virus.
Nonhuman primate models for evaluation of SARS-CoV-2 vaccines
Published in Expert Review of Vaccines, 2022
Jessica A. Neil, Maryanne Griffith, Dale I. Godfrey, Damian F. J. Purcell, Georgia Deliyannis, David Jackson, Steve Rockman, Kanta Subbarao, Terry Nolan
While small animal models can approximate many aspects of human disease and immune responses, NHPs provide the closest approximation to humans based on their genetic, physiological, and immune similarities. For this reason, assessments of immunogenicity and efficacy of vaccines are often undertaken in NHP models prior to advancement to human clinical trials. Like NHPs, hamsters and ferrets are naturally susceptible to SARS-CoV-2 infection and develop respiratory disease, providing valuable small models to study virus transmission and pathology [20,21]. The ancestral strain of SARS-CoV-2 can infect mice expressing human ACE2, through transgenic or viral transduction approaches. Furthermore, adaptation for growth in mice through serial passage has successfully facilitated infection [22,23]. However, naturally occurring variants that carry the N501Y mutation in the receptor binding domain (RBD) of the spike (S) protein can infect mice without adaptation. This mutation occurs in the Alpha, Beta, Gamma, and Omicron but not in the Delta variants [24]. Despite the availability of these small animal models, many preclinical studies for SARS-CoV-2 vaccine candidates focused on NHP models.
Repeated vaccination and ‘vaccine exhaustion’: relevance to the COVID-19 crisis
Published in Expert Review of Vaccines, 2022
Md Anwarul Azim Majumder, Mohammed S. Razzaque
The negative impact of prior immunization on the effectiveness of subsequent vaccination was first observed in British boarding schools by Hoskins et al. and is commonly known as the ‘Hoskins effect’ [11]. The phenomenon has been evidenced in a number of subsequent studies of flu vaccines. For example, the multiyear Canadian Vaccine Effectiveness Network data showed reduced effectiveness in individuals with prior flu vaccination [12]. Importantly, the reduced vaccine effectiveness was more pronounced when identical vaccines were repeated, but the currently circulating virus was a poor antigenic match [12]. In an experimental study, a vaccine developed for the malaria parasite Plasmodium chabaudi showed reduced effectiveness in the absence of parasitic evolution in a serial passage experiment on mice [13].
Murepavadin: a new antibiotic class in the pipeline
Published in Expert Review of Anti-infective Therapy, 2018
Ignacio Martin-Loeches, Glenn E. Dale, Antoni Torres
The potential for resistance development was evaluated through the determination of spontaneous mutation rate and serial passages in liquid media. Murepavadin had a low propensity to induce resistance in vitro, as spontaneous mutation rates on agar plates containing murepavadin at multiples of the MIC were 10–8 to 10–9. In serial passage experiments, P. aeruginosa isolates were inoculated into broth containing the antibiotic at sub-MIC and multiples of the MIC. Drug concentrations were increased during serial passage if bacteria were growing at higher concentration of drug. In all cases the rate of resistance development was compared to standard of care antibiotics including, meropenem, ceftazadime, ciprofloxacin, amikacin and colistin. Murepavadin demonstrated a lower propensity to develop resistance compared to the standard of care antibiotics in vitro. Resistance to murepavadin correlated with mutations in the periplasmic domain of LptD and the murepavadin resistant mutants that were generated remained susceptible to antibiotics currently in clinical use, suggesting that no cross-resistance was observed with other antibiotic classes.