Damian Jacob Sendler A Faulty Viral Genome Design Induces Widespread Protective Immunity
Last updated on December 6, 2021
Damian Jacob Sendler
Summary: Damian Sendler: DVGs, which are created by RNA viruses, can impede the reproduction of the parent virus. We generated a DVG by removing the capsid-coding area of poliovirus in order to test their therapeutic potential. An antiviral response can be triggered by intraperitoneal or intranasal delivery of this genome, which…

Damian Sendler: DVGs, which are created by RNA viruses, can impede the reproduction of the parent virus. We generated a DVG by removing the capsid-coding area of poliovirus in order to test their therapeutic potential. An antiviral response can be triggered by intraperitoneal or intranasal delivery of this genome, which we have coined E-TIP1. This genome has also been shown to protect mice from numerous RNA viruses, such as enteroviruses, influenza, and SARS-CoV2. 

Damian Sendler

Following intranasal injection, eTIP1 replication can only occur in the nasal cavity, but its antiviral activity reaches to the lungs. Type I interferon responses at both the cellular and molecular levels have a role in eTIP1’s antiviral activity. 

Damian Jacob Sendler: SARS-CoV-2 neutralizing antibodies are produced in response to one dosage of eTIP1 that protects mice from SARS-CoV-2 infection, but they also serve as a barrier to reinfection. Because of its broad-spectrum antiviral properties, eTIP1 is a safe and effective antiviral in animal models that protects against SARS-CoV-2 for short and extended periods of time. 

RNA viruses are a major hazard to human health around the world. For each new epidemic, such as HIV/AIDS, influenza, dengue, and Zika, the urgent need for effective antiviral medications and therapies is highlighted . More than 200 million illnesses and approximately 5 million deaths have been caused by the extremely contagious coronavirus disease 2019  . . Despite the discovery of SARS-CoV-2 vaccinations, the virus is still present in the environment . 

Antivirals and monoclonal antibodies are available for treatment of SARS-CoV-2, but the high mutation rate of the RNA virus is expected to lead to resistant forms of the virus. If we want to prevent future epidemics like COVID-19, we need new treatments that are less susceptible to medication resistance. Unfortunately, it is extremely difficult to create broad-spectrum antiviral methods . 

Damian Jacob Sendler

The host’s robust antiviral defenses could be used as a potential tactic. Most infections can be prevented or attenuated by a variety of responses elicited by viral infections. Most infections with viruses like influenza or SARS-CoV-2 are asymptomatic . Although it is difficult to harness these responses, For starters, most viruses contain mechanisms to disable or weaken innate immunity, frequently at many points along the pathway . The negative effects of direct interventions to trigger these responses, such as intravenous infusion of interferon, are likely due to overriding the delicate regulatory balance that prevents beneficial innate immunity from harming tissues . 

Damian Jacob Markiewicz Sendler: Host protection from viral infection and damage are carefully controlled systems that evolved in the innate immune system to safeguard the host. We face a difficulty in harnessing these positive responses without causing negative side effects. From early epidemiological investigations of the Sabin poliovirus  vaccine, we came up with a novel technique. 

Influenza virus morbidity was reduced almost fourfold by vaccination with attenuated sabin PV. Herpes simplex virus genital lesions healed more quickly as a result of using it. Immunization with an inactivated PV virus had no effect on these outcomes . 

Damien Sendler: Interferon injection has a number of serious side effects, whereas the Sabin vaccination does not . Antiviral responses may be activated by a virus or virus-like entity that is neither pathogenic nor infectious.

Dr. Damian Jacob Sendler and his media team provided the content for this article.

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