PXD065873-1

PXD065873 is an original dataset announced via ProteomeXchange.

Title	Coronavirus protein interaction mapping in bat and human cells identifies molecular and genetic switches for immune evasion and replication
Description	Coronaviruses, including SARS-CoV-2, can cause severe disease in humans, whereas reservoir hosts like Rhinolophus bats appear to remain asymptomatic for reasons that are not well-recognized. To understand how host-specific protein-protein interactions (PPIs) shape infection outcomes, we generated comparative PPI maps for SARS-CoV-2 and its close bat-originating relative, RaTG13, using affinity purification-mass spectrometry (AP-MS) in human and Rhinolophus ferrumequinum (RFe) bat cells. Our analysis revealed both conserved as well as virus- and host-specific PPIs, pointing to key interactions that regulate infection dynamics across species. SARS-CoV-2 required a non-synonymous mutation at the RNA-binding domain of the viral N protein to replicate in the RFe bat cells. Moreover, comparative analysis of the viral protein Orf9b revealed differential interactions with the human and bat mitochondrial proteins Tom70 and MTARC2, and modulating virus replication. A single residue in SARS-CoV-2 Orf9b serves as a molecular switch between these interactions, with a T72I substitution weakening Tom70 binding and reducing its ability to counteract innate immune activation. These findings demonstrate how a single-residue substitution can reshape virus-host interactions and contribute to immune evasion and host adaptation.
HostingRepository	PRIDE
AnnounceDate	2026-06-29
AnnouncementXML	Submission_2026-06-28_18:29:22.865.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Danielle Swaney
SpeciesList	scientific name: Homo sapiens (Human); NCBI TaxID: NEWT:9606; scientific name: Severe acute respiratory syndrome coronavirus 2; NCBI TaxID: NEWT:2697049; scientific name: Severe acute respiratory syndrome coronavirus 2; NCBI TaxID: NCBITaxon:2697049; scientific name: Bat coronavirus RaTG13; NCBI TaxID: NEWT:2709072;
ModificationList	No PTMs are included in the dataset
Instrument	Orbitrap Exploris 480; Q Exactive Plus

Revision	Datetime	Status	ChangeLog Entry
0	2025-07-07 18:08:37	ID requested
⏵ 1	2026-06-28 18:29:23	announced

10.1016/j.chom.2026.04.015;

Batra J, Rutkowska M, Zhou Y, Ye C, Adavikolanu R, Young JM, Anand D, Verma S, Parthasarathy H, Gordon M, Malpotra S, Cupic A, Kehrer T, Dos Santos M, Benjamin R, Moen JM, Winters DM, Caval V, Rojc A, Mena I, Aslam S, Martinez-Romero C, Vi, ñ, as IC, Khalil Z, Farrugia K, Villal, ó, n-Letelier F, Banerjee A, Tussia-Cohen D, Diallo A, Maji S, Muralidharan M, Foussard H, Chen IP, Fuchs R, San Felipe CJ, Zuliani-Alvarez L, Choudhury P, Obernier K, Gracias S, Suryawanshi RK, Bonaventure B, Ib, á, ñ, ez C, Johnson JR, Juste J, Pache L, Stroud RM, Verba KA, Fraser JS, van Bakel H, Taha TY, Ott M, Hagai T, Jouvenet N, Demeret C, Polacco BJ, Swaney DL, Echeverria I, Bouhaddou M, Eckhardt M, Malik HS, Martinez-Sobrido L, Miorin L, Garc, í, a-Sastre A, Krogan NJ, Coronavirus protein interaction mapping in bat and human cells reveals network rewiring governing immune evasion and zoonotic potential. Cell Host Microbe, 34(6):1100-1117.e13(2026) [pubmed]

submitter keyword: host-pathogen interactions, RaTG13, SARS-CoV-2,APMS, Bats

Nevan Krogan
contact affiliation	Quantitative Biosciences Institute (QBI), University of California, San Francisco, San Francisco, CA USA J. David Gladstone Institutes, San Francisco, San Francisco, CA, USA Department of Bionengineer and Therapeutic Sciences, University of California, San Francisco, San Francisco, CA, USA
contact email	danielle.swaney@ucsf.edu
lab head
Danielle Swaney
contact affiliation	UCSF
contact email	daniswan@gmail.com
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD065873
     1. Label: PRIDE project
     2. Name: Coronavirus protein interaction mapping in bat and human cells identifies molecular and genetic switches for immune evasion and replication