Association of Nirmatrelvir/Ritonavir Treatment with Long COVID Symptoms in an Online Cohort of Non-Hospitalized Individuals Experiencing Breakthrough SARS-CoV-2 Infection in the Omicron Era

Durstenfeld, Matthew S; Peluso, Michael J.; Lin, Feng; Peyser, Noah D.; Isasi, Carmen R.; Carton, Thomas; Henrich, Timothy J.; Deeks, Steven G.; Olgin, Jeffrey E.; Pletcher, Mark J.; Marcus, Gregory M.; Hsue, Priscilla Y.

doi:10.1101/2023.03.02.23286730

Cited by 4 publications

(3 citation statements)

References 35 publications

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“…While prior SARS-CoV-2 vaccination appears to be protective against the development of PASC (27), it remains unclear whether antiviral treatment during the acute phase of illness might reduce the incidence of this condition. Two studies suggest a benefit among those meeting criteria for antiviral therapy (28,29), but other evaluations have not shown an effect (30,31). Our findings suggest that interventions that alter the magnitude or duration of infectious virus and the associated immune response during the acute phase might have the potential to affect the development of PASC.…”

Section: Discussionmentioning

confidence: 64%

Early Biological Markers of Post-Acute Sequelae of SARS-CoV-2 Infection

Peluso

Glidden

et al. 2023

Preprint

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To understand the roles of acute phase viral dynamics and host immune responses in PASC, we enrolled 136 participants within 5 days of their first positive SARS-CoV-2 real-time PCR. Participants self-collected nasal specimens up to 21 times within the first 28 days after symptom onset; Interviewer-administered clinical questionnaires and blood samples were collected at enrollment and days 9, 14, 21, 28, and month 4 and 8 post-symptom. Defining PASC as the presence of any symptom new or worse since infection reported at their 4-month visit, we compared viral markers (quantity and duration of viral RNA load, infectious viral load, and plasma N-antigen level) and host immune markers (IL-6, IL-10, TNF-a, IFN-a, IFN-g, MCP, IP-10, and Spike IgG) over the acute period. In comparison to those who fully recovered, those who developed PASC demonstrated significantly higher maximum levels of SARS-CoV-2 RNA, infectious virus, and N-antigen, longer duration of viral shedding, and lower Spike-specific IgG levels within the first 10 days of the acute phase of illness. No significant differences were identified among a panel of host immune markers, though there was a trend toward higher initial levels of certain markers (e.g., MCP-1, IFN-a, and IFN-g) in those who went on to develop PASC. Early viral dynamics and the associated host immune responses play a role in the pathogenesis of PASC. These findings highlight the importance of understanding the early biological markers from acute SARS-CoV-2 infection in the natural history of PASC.

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Section: Discussionmentioning

confidence: 64%

Early Biological Markers of Post-Acute Sequelae of SARS-CoV-2 Infection

Peluso

Glidden

et al. 2023

Preprint

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“…The combination of nirmatrelvir with ritonavir has shown potential effectiveness in relief of long COVID symptoms [ 57 ], although other studies did not find evidence to support efficacy of nirmatrelvir in combination with ritonavir (a combination of a SARS-CoV-2 main protease inhibitor [MPro] and an inhibitor of CYP3A4 metabolism) in long-term consequences of COVID [ 58 ].…”

Section: Discussionmentioning

confidence: 99%

Autoimmunity and long COVID in children

Boyarchuk,

Volianska

2024

Reumatologia

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Numerous hypotheses regarding the pathogenetic mechanisms of long COVID have been proposed. Immune dysregulation and autoimmunity are among the leading hypotheses. In this article, we pre-sent two clinical cases of long COVID. The first case demonstrates the phenotype of long COVID with pain and musculoskeletal symptoms, which is often associated with autoimmunity and mimics systemic connective tissue diseases. In the second case, a high titer of antinuclear antibodies was observed after SARS-CoV-2 infection, but the clinical symptoms were limited to fever and headache. Only a comprehensive evaluation of clinical symptoms and thorough objective examination can con-firm or exclude autoimmune diseases after a previous SARS-CoV-2 infection. A systematic search in the PubMed Medline database was carried out for studies focusing on immune dysregulation, auto-immunity, and its association with the clinical phenotype of long COVID. The question of the role of autoimmunity in the development of long COVID and the management approaches are discussed.

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“…Furthermore, those who received Paxlovid for 5 days (n = 35,717) in a recent study among 281,793 patients who had at least 1 risk factor for progression to severe COVID-19 had a 26% lower risk of LC compared with those receiving no antiviral or monoclonal antibody treatment [ 311 ]. Nevertheless, other cohort studies have failed to demonstrate corresponding benefits on long-term COVID sequalae via Paxlovid treatment [ 312 , 313 ].…”

Section: Therapeutic Perspectives and Challengesmentioning

confidence: 99%

Laboratory Findings and Biomarkers in Long COVID: What Do We Know So Far? Insights into Epidemiology, Pathogenesis, Therapeutic Perspectives and Challenges

Tsilingiris

Karampela

Christodoulatos

et al. 2023

IJMS

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Long COVID (LC) encompasses a constellation of long-term symptoms experienced by at least 10% of people after the initial SARS-CoV-2 infection, and so far it has affected about 65 million people. The etiology of LC remains unclear; however, many pathophysiological pathways may be involved, including viral persistence; a chronic, low-grade inflammatory response; immune dysregulation and a defective immune response; the reactivation of latent viruses; autoimmunity; persistent endothelial dysfunction and coagulopathy; gut dysbiosis; hormonal and metabolic dysregulation; mitochondrial dysfunction; and autonomic nervous system dysfunction. There are no specific tests for the diagnosis of LC, and clinical features including laboratory findings and biomarkers may not specifically relate to LC. Therefore, it is of paramount importance to develop and validate biomarkers that can be employed for the prediction, diagnosis and prognosis of LC and its therapeutic response, although this effort may be hampered by challenges pertaining to the non-specific nature of the majority of clinical manifestations in the LC spectrum, small sample sizes of relevant studies and other methodological issues. Promising candidate biomarkers that are found in some patients are markers of systemic inflammation, including acute phase proteins, cytokines and chemokines; biomarkers reflecting SARS-CoV-2 persistence, the reactivation of herpesviruses and immune dysregulation; biomarkers of endotheliopathy, coagulation and fibrinolysis; microbiota alterations; diverse proteins and metabolites; hormonal and metabolic biomarkers; and cerebrospinal fluid biomarkers. At present, there are only two reviews summarizing relevant biomarkers; however, they do not cover the entire umbrella of current biomarkers, their link to etiopathogenetic mechanisms or the diagnostic work-up in a comprehensive manner. Herein, we aim to appraise and synopsize the available evidence on the typical laboratory manifestations and candidate biomarkers of LC, their classification based on pathogenetic mechanisms and the main LC symptomatology in the frame of the epidemiological and clinical aspects of the syndrome and furthermore assess limitations and challenges as well as potential implications in candidate therapeutic interventions.

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Association of Nirmatrelvir/Ritonavir Treatment with Long COVID Symptoms in an Online Cohort of Non-Hospitalized Individuals Experiencing Breakthrough SARS-CoV-2 Infection in the Omicron Era

Cited by 4 publications

References 35 publications

Early Biological Markers of Post-Acute Sequelae of SARS-CoV-2 Infection

Early Biological Markers of Post-Acute Sequelae of SARS-CoV-2 Infection

Autoimmunity and long COVID in children

Laboratory Findings and Biomarkers in Long COVID: What Do We Know So Far? Insights into Epidemiology, Pathogenesis, Therapeutic Perspectives and Challenges

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