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Antiviral therapy for COVID-19: Derivation of optimal strategy based on past antiviral and favipiravir experiences.
Shiraki, Kimiyasu; Sato, Noriaki; Sakai, Kaoru; Matsumoto, Shirou; Kaszynski, Richard H; Takemoto, Masaya.
  • Shiraki K; Senri Kinran University, Suita, Osaka, Japan. Electronic address: k-shiraki@cs.kinran.ac.jp.
  • Sato N; Department of Biomedical Data Intelligence, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
  • Sakai K; Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
  • Matsumoto S; Department of Pediatrics, Graduate School of Medical Sciences, Kumamoto University, Japan.
  • Kaszynski RH; Stanford Solutions, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Takemoto M; Department of Microbiology, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.
Pharmacol Ther ; 235: 108121, 2022 07.
Article in English | MEDLINE | ID: covidwho-1665376
ABSTRACT
Favipiravir, a broad-spectrum RNA-dependent RNA polymerase inhibitor, inhibits the replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) at significantly lower concentrations than the plasma trough levels achieved by the dosage adopted for influenza treatment and exhibits efficacy against coronavirus disease 2019 (COVID-19) pneumonia. Although high doses of favipiravir are required due to the molecule being a purine analog, its conversion into the active form in infected cells with active viral RNA synthesis enhances the antiviral specificity and selectivity as a chain terminator with lethal mutagenesis. Another characteristic feature is the lack of generation of favipiravir-resistant virus. COVID-19 pneumonia is caused by strong cell-mediated immunity against virus-infected cells, and the inflammatory response induced by adaptive immunity continues to peak for 3 to 5 days despite antiviral treatment. This has also been observed in herpes zoster (HZ) and cytomegalovirus (CMV) pneumonia. Inflammation due to an immune response may mask the effectiveness of favipiravir against COVID-19 pneumonia. Favipiravir significantly shortened the recovery time in patients with mild COVID-19 pneumonia by 3 days with the start of treatment by the 5th day of symptom onset. Since both CMV and COVID-19 pneumonia are caused by adaptive immunity and prevention of cytomegalovirus pneumonia is the standard treatment due to difficulties in treating refractory CMV pneumonia, COVID-19 pneumonia should be prevented with early treatment as well. In the present study, we have comprehensively reviewed the optimal antiviral therapy for COVID-19 based on clinical trials of favipiravir for the treatment of COVID-19 pneumonia and the concurrently established therapies for other viral infections, particularly HZ and CMV pneumonia. Optimally, antivirals should be administered immediately after COVID-19 diagnosis, similar to that after influenza diagnosis, to prevent COVID-19 pneumonia and complications resulting from microangiopathy.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Cytomegalovirus Infections / Influenza, Human / COVID-19 Drug Treatment Type of study: Diagnostic study / Prognostic study / Qualitative research Limits: Humans Language: English Journal: Pharmacol Ther Year: 2022 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Cytomegalovirus Infections / Influenza, Human / COVID-19 Drug Treatment Type of study: Diagnostic study / Prognostic study / Qualitative research Limits: Humans Language: English Journal: Pharmacol Ther Year: 2022 Document Type: Article