Evidence map›Paper›PMID 36265309›Full record

ReviewBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2022

The role of SARS-CoV-2 accessory proteins in immune evasion.

Milad Zandi, Maryam Shafaati, Davood Kalantar-Neyestanaki, Hossein Pourghadamyari, Mona Fani, Saber Soltani, Hassan Kaleji, Samaneh Abbasi

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 88 citations in OpenAlex.

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  7. Host Responses to SARS-CoV-2 with an Emphasis on Cytokines.International journal of molecular sciences · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Milad ZandiDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: mzandi@razi.tums.ac.ir.
Maryam ShafaatiDepartment of Microbiology, Faculty Science, Jahrom Branch, Islamic Azad University, Jahrom, Iran; Occupational Sleep Research Center, Baharloo Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Davood Kalantar-NeyestanakiMedical Mycology and Bacteriology Research Center, Kerman University of Medical Sciences, Kerman, Iran; Department of Medical Microbiology (Bacteriology & Virology), Afzalipour Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Hossein PourghadamyariStudent Research Committee, Kerman University of Medical Sciences, Kerman, Iran; Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Mona FaniDepartment of Pathobiology & Laboratory Sciences, School of Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran.
Saber SoltaniDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Hassan KalejiDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Samaneh AbbasiDepartment of Microbiology, School of Medicine, Abadan University of Medical Sciences, Abadan, Iran. Electronic address: s.abbasi@abadanums.ac.ir.
Tehran University of Medical Sciences · IRKerman University of Medical Sciences · IRJahrom University · IRNorth Khorasan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many questions on the SARS-CoV-2 pathogenesis remain to answer. The SARS-CoV-2 genome encodes some accessory proteins that are essential for infection. Notably, accessory proteins of SARS-CoV-2 play significant roles in affecting immune escape and viral pathogenesis. Therefore SARS-CoV-2 accessory proteins could be considered putative drug targets. IFN-I and IFN-III responses are the primary mechanisms of innate antiviral immunity in infection clearance. Previous research has shown that SARS-CoV-2 suppresses IFN-β by infecting host cells via ORF3a, ORF3b, ORF6, ORF7a, ORF7b, ORF8, and ORF9b. Furthermore, ORF3a, ORF7a, and ORF7b have a role in blocking IFNα signaling, and ORF8 represses IFNβ signaling. The ORF3a, ORF7a, and ORF7b disrupt the STAT1/2 phosphorylation. ORF3a, ORF6, ORF7a, and ORF7b could prevent the ISRE promoter activity. The main SARS-CoV-2 accessory proteins involved in immune evasion are discussed here for comprehensive learning on viral entry, replication, and transmission in vaccines and antiviral development.

Indexed as

COVID-19SARS-CoV-2Antiviral AgentsHumansImmune EvasionInterferon-betaAntiviral AgentsInterferon-betaAccessory proteinsImmune evasionORFSARS-CoV-2

Identifiers

PMID36265309
PMCPMC9574935
OpenAlexW4306405700

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.