Evidence map›Paper›PMID 40552037›Full record

ReviewPeerJ2025

Innate immunity, therapeutic targets and monoclonal antibodies in SARS-CoV-2 infection.

Mubashir Nazir, Ishfaq Rashid Mir, Shabir Ahmad Lone, Ghazala Muteeb, Ragib Alam, Anis Bashir Fomda, Nida Khan, Asim Azhar, Bashir Ahmad Fomda, Wajihul Hasan Khan

Abstract readReview
In one paragraph

Review in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Mubashir NazirDepartment of Microbiology, Sher-I-Kashmir Institute of Medical Sciences Soura, Srinagar, Jammu and Kashmir, India.
Ishfaq Rashid MirDepartment of Immunology and Molecular Medicine, Sher-I-Kashmir Institute of Medical Sciences Soura, Srinagar, Jammu and Kashmir, India.
Shabir Ahmad LoneDepartment of Microbiology, Sher-I-Kashmir Institute of Medical Sciences Soura, Srinagar, Jammu and Kashmir, India.
Ghazala MuteebDepartment of Nursing, College of Applied Medical Science, King Faisal University, Al-Ahsa, Saudi Arabia.
Ragib AlamDepartment of Microbiology, All India Institute of Medical Sciences, New Delhi, Delhi, India.
Anis Bashir FomdaDepartment of Psychiatry, All India Institute of Medical Sciences, New Delhi, Delhi, India.
Nida KhanDepartment of Chemical Engineering, Indian Institute of Technology, Delhi, New Delhi, India.
Asim AzharInterdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, Uttar Pradesh, India.
Bashir Ahmad FomdaDepartment of Microbiology, Sher-I-Kashmir Institute of Medical Sciences Soura, Srinagar, Jammu and Kashmir, India.
Wajihul Hasan KhanDepartment of Microbiology, All India Institute of Medical Sciences, New Delhi, Delhi, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 (coronavirus disease 2019), caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), stands as one of the most severe pandemics the world has ever faced in recent times. SARS-CoV-2 infection exhibits a wide range of symptoms, varying from severe manifestations to mild cases and even asymptomatic carriers. This diversity stems from a multitude of factors, including genetic predisposition, viral variants, and immune status. During SARS-CoV-2 infection, the immune system engages pattern recognition receptors, setting off a series of intricate signalling cascades. These cascades culminate in the activation of innate immune responses, including induction of type I and type III interferons. The emerging variants of SARS-CoV-2 pose challenges to the innate immune system defense. Therefore, investigating the innate immune response is crucial for effectively combating SARS-CoV-2 and its variants. The cyclic guanosine monophosphate-adenosine monophoshate synthase-stimulator of interferon genes (cGAS-STING) pathway, a critical innate immune mechanism, represents a promising target for intervention at multiple stages to reduce the severity and progression of SARS-CoV-2 infection. This review explores innate immunity in SARS-CoV-2 infection and other immune responses critical for SARS-CoV-2 defence. As part of the therapeutic approach, we extend our review to highlight monoclonal antibodies (mAbs) as emerging and effective therapeutics for controlling SARS-CoV-2 by targeting different stages of the innate immune system. A diverse range of mAbs has been explored to address specific targets within the innate immune pathways. A deep understanding of innate immunity and targeted monoclonal therapeutics will be instrumental in combating viruses and their variants, laying the foundation for enhanced treatment and therapeutic strategies.

Indexed as

Antibodies, MonoclonalCOVID-19COVID-19 Drug TreatmentImmunity, InnateSARS-CoV-2Antiviral AgentsHumansAntibodies, MonoclonalAntiviral AgentsInnate immunityMonoclonal antibodySARS-CoV-2Signaling moleculesSTINGs

Identifiers

PMID40552037
PMCPMC12184675

What OpenQuestion holds

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LicenceCC BY
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.