Evidence map›Paper›PMID 34566457›Full record

ArticleSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2021

SAR-CoV-2 infection, emerging new variants and the role of activation induced cytidine deaminase (AID) in lasting immunity.

Asad Ullah, Neelam Mabood, Muhammad Maqbool, Luqman Khan, Maria Khan, Mujib Ullah

Open access · hybridAbstract read
In one paragraph

Article in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Biomolecules · 2023
    Article
  2. Review
  3. A Long-Running Arms Race betweenJournal of virology · 2023
    Article
  4. Role of CD9 Sensing, AI, and Exosomes in Cellular Communication of Cancer.International journal of stem cell research and therapy · 2023
    Article
  5. Article
  6. Review
  7. Article
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

6 authors at 4 institutions in 2 countries.

Asad UllahDepartment of Radiation Oncology, School of Medicine, University of California San Francisco, San Francisco, CA, USA.
Neelam MaboodDepartment of Pediatrics, University of Alberta, Edmonton, Alberta, Canada.
Muhammad MaqboolDepartment of Clinical & Diagnostic Sciences, The University of Alabama at Birmingham, Birmingham, AL, USA.
Luqman KhanCardiovascular Vascular Research Institute, School of Medicine, University of California San Francisco, San Francisco, CA, USA.
Maria KhanDepartment of Immunology and Transplantation, School of Medicine, Stanford University, Stanford, CA, USA.
Mujib UllahDepartment of Immunology and Transplantation, School of Medicine, Stanford University, Stanford, CA, USA.
Stanford University · USUniversity of California, San Francisco · USUniversity of Alabama at Birmingham · USUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the world faces a fourth COVID-19 spike, scientists are learning a lot more about the new SARS-CoV-2 strains that were previously unknown. Currently, the Delta versions of SARS-CoV-2 have become the prevalent strains in much of the world since it first appeared in India in late 2020. Researchers believe they have discovered why Delta has been so successful: those infected with it create significantly more virus than those infected with the original strain of SARS-CoV-2, making it extremely contagious. This has redirected the focus to how our immune system defends us from these various pathogens and initiates such varied responses. Hundreds of research papers have been published on the origins of long-lasting immune responses and disparities in the numbers of different immune cell types in COVID 19 survivors, but the primary architect of these discrepancies has yet to be discovered. In this essay, we will concentrate on the primary architect protein, activation induced cytidine deaminase (AID), which triggers molecular processes that allow our immune system to produce powerful antibodies and SARS-CoV-2 specific B cells, allowing us to outwit the virus. We believe that if we ever achieve permanent immunity to SARS-CoV-2 infection, AID will be the key to releasing it.

Indexed as

Cytidine deaminaseNew variants of CoronavirusPerpetual immunitySRS-CoV-2

Identifiers

PMID34566457
PMCPMC8452370
OpenAlexW3199393288

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.