Molnupiravir clinical trial simulation suggests that polymerase chain reaction underestimates antiviral potency against SARS-CoV-2 DOI Creative Commons
Shadisadat Esmaeili, Katherine Owens, Joseph F. Standing

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 22, 2024

Molnupiravir is an antiviral medicine that induces lethal copying errors during SARS-CoV-2 RNA replication. reduced hospitalization in one pivotal trial by 50% and had variable effects on reducing viral levels three separate trials. We used mathematical models to simulate these trials closely recapitulated their virologic outcomes. Model simulations suggest lower potency against pre-omicron variants than omicron. estimate vitro assays underestimate vivo 7-8 fold omicron variants. Our model suggests because polymerase chain reaction detects molnupiravir mutated variants, the true reduction non-mutated underestimated ∼0.5 log 10 two conducted while dominated. Viral area under curve estimates differ significantly between RNA. results reinforce past work suggesting are unreliable for estimating drug endpoints respiratory virus clinical should be catered mechanism of action.

Язык: Английский

A unifying model to explain frequent SARS-CoV-2 rebound after nirmatrelvir treatment and limited prophylactic efficacy DOI Creative Commons
Shadisadat Esmaeili, Katherine Owens,

Jessica Wagoner

и другие.

Nature Communications, Год журнала: 2024, Номер 15(1)

Опубликована: Июнь 28, 2024

Abstract In a pivotal trial (EPIC-HR), 5-day course of oral ritonavir-boosted nirmatrelvir, given early during symptomatic SARS-CoV-2 infection (within three days symptoms onset), decreased hospitalization and death by 89.1% nasal viral load 0.87 log relative to placebo in high-risk individuals. Yet, nirmatrelvir/ritonavir failed as post-exposure prophylaxis trial, frequent rebound has been observed subsequent cohorts. We develop mathematical model capturing viral-immune dynamics nirmatrelvir pharmacokinetics that recapitulates loads from this another clinical (PLATCOV). Our results suggest nirmatrelvir’s vivo potency is significantly lower than vitro assays predict. According our model, maximally potent agent would reduce the approximately 3.5 logs at 5 days. The identifies earlier initiation shorter treatment duration are key predictors post-treatment rebound. Extension 10 for Omicron variant vaccinated individuals, rather increasing dose or dosing frequency, predicted incidence significantly.

Язык: Английский

Процитировано

8

Modeling suggests SARS-CoV-2 rebound after nirmatrelvir-ritonavir treatment is driven by target cell preservation coupled with incomplete viral clearance DOI Creative Commons
Tin Phan, Ruy M. Ribeiro,

Gregory E. Edelstein

и другие.

Journal of Virology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 4, 2025

ABSTRACT In a subset of SARS-CoV-2-infected individuals treated with the antiviral nirmatrelvir-ritonavir, virus rebounds following treatment. The mechanisms driving this rebound are not well understood. We used mathematical model to describe longitudinal viral load dynamics 51 20 whom rebounded. Target cell preservation, either by robust innate immune response or initiation N-R near time symptom onset, coupled incomplete clearance, appears be main factor leading rebound. Moreover, occurrence is likely influenced treatment relative progression infection, earlier treatments higher chance A comparison an untreated cohort suggests that early nirmatrelvir-ritonavir may associated delay in onset adaptive response. Nevertheless, our demonstrates extending course 10-day regimen greatly diminish people mild-to-moderate COVID-19 and who at high risk severe disease. Altogether, results suggest some individuals, standard 5-day starting around completely eliminate virus. Thus, after ends, can if effective has fully developed. These findings on role target preservation clearance also offer possible explanation for other SARS-CoV-2. IMPORTANCE Nirmatrelvir-ritonavir initial reduction followed once stopped. show timing influence stops growth preserves cells but lead full adequately developed, remaining Our provide insights into help develop better strategies minimize possibility.

Язык: Английский

Процитировано

0

Management of SARS-CoV-2 Infection-Clinical Practice Guidelines of the Polish Association of Epidemiologists and Infectiologists, for 2025 DOI Open Access
Robert Flisiak, Jerzy Jaroszewicz, Dorota Kozielewicz

и другие.

Journal of Clinical Medicine, Год журнала: 2025, Номер 14(7), С. 2305 - 2305

Опубликована: Март 27, 2025

The first Polish recommendations for the management of COVID-19 were published by Society Epidemiologists and Infectiologists (PTEiLChZ) on 31 March 2020, last three years ago. emergence new SARS-CoV-2 variants, a different course disease, as well knowledge about therapies vaccines, requires updating diagnostic, therapeutic, prophylactic guidelines. Despite reduction in threat associated with COVID-19, there is risk another epidemic caused coronaviruses, which was an additional reason developing version In preparing these recommendations, Delphi method used, reaching consensus after survey cycles. Compared to 2022 version, names individual stages disease have been changed, adapting them realities clinical practice, attention paid differences observed immunosuppressed patients children. Some previously recommended drugs discontinued, including monoclonal antibodies. addition, general principles vaccination presented, issues related post-COVID syndrome.

Язык: Английский

Процитировано

0

Modeling suggests SARS-CoV-2 rebound after nirmatrelvir-ritonavir treatment is driven by target cell preservation coupled with incomplete viral clearance DOI Creative Commons
Tin Phan, Ruy M. Ribeiro,

Gregory E. Edelstein

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Сен. 16, 2024

Abstract In a subset of SARS-CoV-2 infected individuals treated with the oral antiviral nirmatrelvir-ritonavir, virus rebounds following treatment. The mechanisms driving this rebound are not well understood. We used mathematical model to describe longitudinal viral load dynamics 51 20 whom rebounded. Target cell preservation, either by robust innate immune response or initiation nirmatrelvir-ritonavir near time symptom onset, coupled incomplete clearance, appear be main factors leading rebound. Moreover, occurrence is likely influenced treatment relative progression infection, earlier treatments higher chance Finally, our demonstrates that extending course treatment, in particular 10-day regimen, may greatly diminish risk for people mild-to-moderate COVID-19 and who at high severe disease. Altogether, results suggest some individuals, standard 5-day starting around onset completely eliminate virus. Thus, after ends, can if an effective adaptive has fully developed. These findings on role target preservation clearance also offer possible explanation other SARS-CoV-2. Importance Nirmatrelvir-ritonavir initial reduction followed once stopped. show timing influence stops growth preserves cells but lead full adequately developed, remaining Our provide insights into help develop better strategies minimize possibility.

Язык: Английский

Процитировано

1

Coronavirus Disease 2019 Rebound in Nirmatrelvir Plus Ritonavir Treatment and Control Groups: A Prospective Cohort Study DOI Creative Commons
Jacqueline K. Kueper,

Kalyani Kottilil,

Giorgio Quer

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 6, 2024

Abstract Observation of COVID-19 rebound after Nirmatrelvir Plus Ritonavir (NPR) has driven important questions surrounding one the only direct acting antiviral treatments for COVID-19. This prospective cohort study to investigate incidence enrolled 917 positive outpatients via a digital proctored test-to-treat solution. Among 669 included in evaluation 493 intended take NPR and 176 did not. Participants were provided frequent tests symptom surveys 15 days. Time initial viral or clearance was not different between groups. Overall, 15-day three-fold higher group (15.2% vs 5.4%, p <0.001) double (16.4% 8.4%, <0.01). those experiencing resolution, resolution notably (43.8% 17.5%). demonstrates that while occurs both treated untreated outpatients, is group.

Язык: Английский

Процитировано

1

Meeting Report of the 37th International Conference on Antiviral Research in Gold Coast, Australia, May 20–24, 2024, organized by the International Society for Antiviral Research DOI
Stephen R. Welch, John P. Bilello, Kara Carter

и другие.

Antiviral Research, Год журнала: 2024, Номер 232, С. 106037 - 106037

Опубликована: Ноя. 13, 2024

Язык: Английский

Процитировано

0

A theory for viral rebound after antiviral treatment: A study case for SARS-CoV-2 DOI
Mara Pérez, Marcelo Actis, Ignacio José García Sánchez

и другие.

Mathematical Biosciences, Год журнала: 2024, Номер unknown, С. 109339 - 109339

Опубликована: Ноя. 1, 2024

Язык: Английский

Процитировано

0

Molnupiravir clinical trial simulation suggests that polymerase chain reaction underestimates antiviral potency against SARS-CoV-2 DOI Creative Commons
Shadisadat Esmaeili, Katherine Owens, Joseph F. Standing

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 22, 2024

Molnupiravir is an antiviral medicine that induces lethal copying errors during SARS-CoV-2 RNA replication. reduced hospitalization in one pivotal trial by 50% and had variable effects on reducing viral levels three separate trials. We used mathematical models to simulate these trials closely recapitulated their virologic outcomes. Model simulations suggest lower potency against pre-omicron variants than omicron. estimate vitro assays underestimate vivo 7-8 fold omicron variants. Our model suggests because polymerase chain reaction detects molnupiravir mutated variants, the true reduction non-mutated underestimated ∼0.5 log 10 two conducted while dominated. Viral area under curve estimates differ significantly between RNA. results reinforce past work suggesting are unreliable for estimating drug endpoints respiratory virus clinical should be catered mechanism of action.

Язык: Английский

Процитировано

0