Evidence map›Paper›PMID 42095660›Full record

ArticleJournal of virology2026

Replication-competent SIVcpz CRISPR screen identifies barriers to successful cross-species transmission.

Qinya Xie, Qingxing Wang, Sabrina Noettger, Guillermo Gosálbez, Annika C Betzler, Meta Volcic, Dorota Kmiec, Stefan Krebs, Alexander Graf, Dila Gülensoy and 3 more

Abstract read
In one paragraph

Article in Journal of virology, 2026. 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

13 authors.

Qinya Xie *Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Qingxing Wang *Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Sabrina Noettger *Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Guillermo Gosálbez *Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Annika C BetzlerInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Meta VolcicInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Dorota KmiecInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.ORCID 0000-0001-7302-6015
Stefan KrebsLaboratory for Functional Genome Analysis, Gene Center, LMU Munich, Munich, Germany.
Alexander GrafLaboratory for Functional Genome Analysis, Gene Center, LMU Munich, Munich, Germany.
Dila GülensoyInstitute of Biochemistry and Molecular Biology, Ulm University, Ulm, Germany.
Gilbert WeidingerInstitute of Biochemistry and Molecular Biology, Ulm University, Ulm, Germany.
Konstantin M J SparrerInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Frank KirchhoffInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.ORCID 0000-0002-7052-2360

Funding

Deutsche Forschungsgemeinschaft KI 548/21-1, VO 2829/2-1European Research Council 101054456
6 · The paper itself

Abstract

Simian immunodeficiency viruses (SIVs) have crossed from apes to humans at least four times, but only one event gave rise to the AIDS pandemic. The host barriers that pandemic HIV-1 group M ( IMPORTANCE: Four independent transmission events of simian immunodeficiency viruses from chimpanzees and gorillas to humans gave rise to human immunodeficiency virus type 1, but only one led to the global AIDS pandemic. Understanding which adaptations allowed the pandemic HIV-1 M strains to spread efficiently in humans remains a key question in virus evolution and public health. In this study, we engineered replication-competent SIVcpz constructs carrying more than 1,500 single-guide RNAs to identify antiviral genes in Cas9-expressing cells. This approach revealed several cellular factors that restrict SIVcpz but not the pandemic HIV-1 M strains analyzed in primary human T cells. These findings provide new insights into antiviral defense mechanisms and the adaptations that most likely contributed to the efficient spread of HIV-1.

Indexed as

CRISPR-Cas SystemsSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusVirus ReplicationAnimalsHIV-1HumansPan troglodytesAXIN1IFITM2MEFVPCED1Breplication-competent CRISPR screenSIVcpz

Identifiers

PMID42095660
PMCPMC13288819

What OpenQuestion holds

Textmetadata
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.