Host-Parasite Relationships
Julius P. Kreier in Infection, Resistance, and Immunity, 2022
One of the more unique mechanisms for spread of a parasite, and one which is damaging to the host, was developed by the neurotrophic rabies virus. The virus, which grows in the host′s brain and its salivary glands, causes changes in the host′s behavior so that it attacks other potential hosts, inoculating infected saliva during the attack. In most of the host species of the rabies virus, the damage to the nervous system that causes these changes is finally fatal to the host. However, in bats and skunks, which are probably the hosts in which the rabies virus maintains itself between epidemics, damage is limited and spread is not dependent on changes in the host′s behavior. The occurrence of some damage as a result of parasitization does not change the fact that it is usually not in the interest of a parasite to severely damage its host.
Bacteria are harmless
Dinesh Kumar Jain in Homeopathy, 2022
In example one, Hahnemann observed that after a dog bite, part was cleaned and removed from the body still the patient suffered from hydrophobia and died. That's why he concluded that external microorganisms were not responsible for hydrophobia and death. Then he presumed that the cause of hydrophobia was within the person and not related to dog bite. Truth was missed by Hahnemann. But it was the reality. Rabies, also known as hydrophobia, is an acute highly fatal viral disease of the central nervous system. It is transmitted to man by bites or licks of rabid animals. Rabies virus spreads from the site of infection via the peripheral nerves toward the central nervous system. Bite wounds should not be immediately sutured to prevent extra trauma, which may help spread the virus into the deeper tissues (Park, 1997, pp. 207–210). In this example, dissection at the site of dog bite exposed nerve endings that facilitated virus transmission to the central nervous system. “Once the virus reaches the central nervous system, it replicates almost exclusively within the gray matter and then passes centrifugally along autonomic nerves to reach other tissue” (Corey, 1983, p. 1136), causing death.
Neuroviral Infections
Sunit K. Singh, Daniel Růžek in Neuroviral Infections, 2013
As to neuroviral infections, the importance of surface receptors was first emphasized by Holland and McLaren for polioviruses (Holland 1961; Holland and McLaren 1961). For the concept of neurotropism, it was an important step forward when Lentz et al. (1982) published their observation that nicotinic acetylcholine receptors at the neuromuscular junction may serve as portals of entry for rabies virus, a strict neu-rotropic agent. Binding the rabies virus to the chick neuromuscular junction could be prevented by α-bungarotoxin and d-tubocurarine. Soon thereafter, on the basis of tissue culture studies, doubt was cast on the acetylcholine receptor hypothesis (Reagan and Wunner 1985). Despite these doubts, this hypothesis has been widely accepted, since it offers a plausible explanation for the affinity of rabies virus to motor nerve endings and striated muscle and for the very wide host range of the agent.
Multi-Patient Rabies Exposure on a Colorado River Rafting Expedition: Urgent vs. Emergent Transport Decision Making in an Austere Setting
Published in Prehospital Emergency Care, 2018
Emily A. Pearce, Aaron N. Farney, Laura Banks, Andrew J. Harrell
Once introduced to a human or animal via a bite or other exposure, the rabies virus travels proximally along the neurons of the peripheral nervous system until it reaches the CNS.20 The time during which the virus travels along the peripheral nervous system is called the incubation period. The incubation period is highly variable, ranging from 1 week to 3 months and as long as 1 year.4,20 The duration of the incubation period is directly affected by the bite location; the farther the bite is located from the CNS, the longer the incubation period.20 Hence, a patient who sustained a bite in the foot will have a longer window before becoming symptomatic than a victim who was bitten in the face. During the incubation period, the infected person or animal is neither symptomatic nor capable of transmitting the disease.20 It is during this time that rabies can be treated and halted from progressing.
Current status of human rabies prevention: remaining barriers to global biologics accessibility and disease elimination
Published in Expert Review of Vaccines, 2019
Charles E. Rupprecht, Naseem Salahuddin
While not ignoring the limitations of overall supply availability in LDCs, the basic quality of current biologics, as evident in Table 1, is more than adequate to meet the basic goals of the GEHRD program [17,79,80]. Future products would obviously benefit the global initiative, if able to meet the cost and schedule recommendations needed for LDCs, using a variety of realistic approaches [92]. Today, highly purified, serum-free, thermo-stable Vero cell-based vaccines are poised to become the next major human rabies product to be licensed in over 40 years [93]. Other approaches will take longer. For example, simian-based recombinant adenovirus vaccines, expressing the rabies virus glycoprotein, have demonstrated pre-clinical safety and efficacy after a single administration, in comparison to conventional-licensed biologics [94]. Additionally, phase one human clinical trials have begun with rabies virus RNA as an immunogen [95]. An imaginative tactic of using flaviviruses as a platform to express rabies virus glycoprotein could fill some major NTD needs, for both the New and Old World Tropics alike [96,97]. Recombinant rabies virus vectors also offer opportunities for human and veterinary interventions, such as combined vaccines against rabies and hemorrhagic fever viruses, as well as options for oral immunization of both wildlife and dogs [98,99].
Adjuvant activity of ethanol extract of Hippophae rhamnoides leaves with inactivated rabies virus antigen
Published in Pharmaceutical Biology, 2018
D. Singh, B. Jayashankar, K. P. Mishra, H. Tanwar, S. N. Madhusudana, A. Y. Belludi, R. Tulsawani, S. B. Singh, L. Ganju
In rabies virus vaccination, it is widely accepted that neutralizing Abs are essential for protection but experimental infections in mice suggest that cell-mediated immune responses are required for efficient viral clearance (Johnson et al. 2010). The contribution of T cells to antiviral immunity in humans has been well established for many viral pathogens. CD8+ T cells follow a program of proliferation and differentiation into CTL armed with effector functions that facilitate pathogen clearance or containment. The CTLs utilize granzymes and perforins to kill virus-infected cells as a major line of defence (Rock et al. 2005). After viral clearance, a pool of virus-specific memory CD8+ T cells survive long term in the host (Byers et al. 2003). A subset of CD8+ T cells, called the resting memory T cell population are designated as CD62LhiCD44hi (Singh 2007). Our study also showed that CD8+ Granzyme B+ CTL (Figure 7) and the resting memory T cell populations (Table 1) increased in SBTE-rabies antigen immunized group compared to that in rabies antigen immunized group.
Related Knowledge Centers
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