ReviewCells2021
The Molecular Interplay between Human Coronaviruses and Autophagy.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Review
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- ELV-N34, RvD6-Isomer, or NPD1 Halt Replication of SARS-CoV-2 Omicron BA.5 Virus in Human Lung and Nasal Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Unlocking the Potential of RNA Sequencing in COVID-19: Toward Accurate Diagnosis and Personalized Medicine.Diagnostics (Basel, Switzerland) · 2025Review
- Selection and characterization of human scFvs targeting the SARS-CoV-2 nucleocapsid protein isolated from antibody libraries of COVID-19 patients.Scientific reports · 2024Article
- Highly Twisted Conformation Thiopyrylium Photosensitizers for In Vivo Near Infrared-II Imaging and Rapid Inactivation of Coronavirus.Angewandte Chemie (International ed. in English) · 2023Article
- Severe acute respiratory syndrome coronavirus-2 accessory proteins ORF3a and ORF7a modulate autophagic flux and CaFrontiers in microbiology · 2023Article
- COVID-19 and hepatorenal syndrome.World journal of gastroenterology · 2022Review
- RNA sequence analysis of nasopharyngeal swabs from asymptomatic and mildly symptomatic patients with COVID-19.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022Article
- Review
- SARS-CoV-2: A Master of Immune Evasion.Biomedicines · 2022Review
- Article
- Autophagy in Viral Infection and Pathogenesis.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Coronavirus disease 2019 (COVID-19), caused by a new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has instantaneously emerged as a worldwide pandemic. However, humans encountered other coronaviruses in the past, and they caused a broad range of symptoms, from mild to life-threatening, depending on the virus and immunocompetence of the host. Most human coronaviruses interact with the proteins and/or double-membrane vesicles of autophagy, the membrane trafficking pathway that degrades and recycles the intracellular protein aggregates, organelles, and pathogens, including viruses. However, coronaviruses often neutralize and hijack this pathway to complete their life cycle. In this review, we discuss the interactions of human coronaviruses and autophagy, including recent data from SARS-CoV-2-related studies. Some of these interactions (for example, viral block of the autophagosome-lysosome fusion), while being conserved across multiple coronaviruses, are accomplished via different molecular mechanisms. Therefore, it is important to understand the molecular interplay between human coronaviruses and autophagy for developing efficient therapies against coronaviral diseases.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.