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Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
Successful parasites must survive long enough within their hosts to develop, reproduce and otherwise complete their life cycle. To do so, they must avoid immune destruction, at least until transmission is complete. This fact of life for any parasite is one of the critical factors determining host range. If immune-mediated elimination is too immediate or complete, a potential host is simply off-limits as far as the parasite is concerned.
Host-Parasite Relationships
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Restriction in host range may be a serious handicap to the study of some human pathogens. The third postulate cannot be fulfilled if no suitable experimental host is available. Until recently, for example, no experimental host could be infected with Hanson′s bacillus (Mycobacterium leprae). This prevented fulfillment of the third postulate for leprosy. Today it is known that the organism will grow in the armadillo. Even when an experimental host has been found in which an organism may grow, the disease produced may not resemble that in the definitive host. These are a few of the factors limiting the utility of Koch′s Postulates, or at least making it necessary to consider their application with some discretion.
Remote Sensing and Computational Epidemiology
Published in Abbas Rajabifard, Greg Foliente, Daniel Paez, COVID-19 Pandemic, Geospatial Information, and Community Resilience, 2021
Viruses spread in many ways. One transmission pathway is through disease-bearing organisms known as vectors: for example, viruses are often transmitted from plant to plant by insects that feed on plant sap, such as aphids; and viruses in animals can be carried by blood-sucking insects and vampire bats. The infectious dose required to produce infection in humans is less than 100 particles in Influenza viruses [11, 12] and to some extent in COVID-19. The variety of host cells that a virus can infect is called its “host range”. This can be narrow or broad, meaning a virus is capable of infecting only few species, or infecting many.
Emerging Human Coronavirus Infections (SARS, MERS, and COVID-19): Where They Are Leading Us
Published in International Reviews of Immunology, 2021
The S protein is a class 1 fusion protein, which promotes attachment and fusion of the viral and cellular membrane to facilitate the virus entry in the cell [197]. Hence S protein determines the host range and cell tropism. The S protein is a homotrimer comprising of 3 protomers, each comprises of single polypeptide chain of 1100–1600 residues, depending on the CoV species [57]. For many CoVs, the S protein is cleaved into S1 and S2 functional units by host cell proteases, which remain non-covalently bound in the prefusion conformation [197]. Also, the core structures of MERS-CoV and SARS-CoV S1-CTDs are similar to each other, whereas their receptor binding motifs (RBMs) are markedly different [198]. For example, SARS-CoV RBM is a loop-dominated gentle concave surface, whereas MERS-CoV RBM has a four-stranded antiparallel β-sheet to provide a relatively flat surface for DPP4 binding [198]. Like, SARS-CoV RBM, the SARS-CoV-2 RBM forms a gently concave surface with a ridge on one side, which binds to the exposed outer surface of the claw-like structure of ACE2 [43]. The binding interface of SARS-CoV2 RBM is bigger than the SARS-CoV RBM and covers more ACE2 surface. The conservation of glycan interacting arginine between SARS-CoV and SARS-CoV2 in their ACE2 binding cites shows a close evolutionary relationship between two viruses [43].
An overview of tecovirimat for smallpox treatment and expanded anti-orthopoxvirus applications
Published in Expert Review of Anti-infective Therapy, 2021
Andrew T. Russo, Douglas W. Grosenbach, Jarasvech Chinsangaram, Kady M. Honeychurch, Paul G Long, Candace Lovejoy, Biswajit Maiti, Ingrid Meara, Dennis E. Hruby
Animal models of smallpox are especially challenging in that the host range of VARV is restricted to humans. VARV-induced lethal disease is difficult to achieve in non-human primates, requiring high viral challenge doses (108–109 PFU) and routes of infection that are not biologically relevant [60]. The disease resulting from intravenous VARV challenge poorly mimics the clinical characteristics of classic human smallpox at the higher challenge dose, more closely resembling the rare hemorrhagic presentation (reviewed in [61]). At the lower challenge dose (108 PFU), intravenous VARV challenge results in disease that resembles classic human smallpox following the asymptomatic incubation period, just after the prodromal stage of disease (see Figure 3 for timeline of human smallpox pathology), and is approximately 30% lethal [62]. The low mortality observed in this model, the requirement that VARV studies would have to be conducted at the USCDC, and the limited animal capacity in the USCDC ABSL-4 make the design and conduct of studies with sufficient statistical power to evaluate efficacy of antivirals against VARV in the intravenous challenge model of VARV in NHPs prohibitive.
A review of phage mediated antibacterial applications
Published in Alexandria Journal of Medicine, 2021
Kenneth Ssekatawa, Denis K. Byarugaba, Charles D. Kato, Eddie M. Wampande, Francis Ejobi, Robert Tweyongyere, Jesca L. Nakavuma
Specificity restricts phage infections to only certain bacteria with corresponding receptors to which they can bind; this determines the phage’s host range [48]. For that reason, the application of phage therapy relies on an accurate characterization of all the strains, pathotypes, and serotypes of the target bacteria. Interestingly, if phage therapy overcomes the current obstacles hindering its approval universally, single phage and phage cocktail formulations must be designed indicating the pharmaceutical dosage and the phage host range for a given bacteria which calls for robust characterization of given target host bacteria. Conversely, this review identified gross deviation from the recommended procedure if meaningful phage therapy outcomes are to be achieved as only 55.8% (53) of studies reviewed attempted to use identified bacterial host strains, serovars, and pathotypes, Table 1–5. Worst still, no human in vivo phage therapy trial reported characterization of the target bacteria to their strains, pathotypes, and serotypes. Nevertheless, the spectrum and efficacy of phages can be enhanced by the use of phage cocktails. Phage cocktails also present another advantage of preventing phage resistance [49,50].