Using Bacterial Effectors to Uncover Innate Immune Mechanisms Restricting Viral Replication in Bat Cells

NIH Pandemic-Era Grants

Pandemic Era Grants

2024

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Principal Investigator: Don Brad Gammon
Organization: UT SOUTHWESTERN MEDICAL CENTER
Fiscal Year: 2024
Award: $205,000
Funding agency: National Institute of Allergy and Infectious Diseases

Project Summary 
  Bats are important reservoirs for diverse viral pathogens affecting humans. However, we have a poor 
understanding  of the  key bat  innate  immunity factors  that  restrict  virus  replication.  Functional  assays  that  can 
identify  bat  factors  that  are  truly  relevant  to  combating  viruses  are  needed  to  understand  the  innate  immune 
mechanisms that ultimately define bat susceptibility to viral infection. While historically such functional screens 
have  relied  on  genome-­wide  genomic  editing  (e.g.  CRISPR-­Cas9)-­  or  RNA  interference  (RNAi)-­based 
techniques, such platforms are unavailable for most bat species. Thus, new methods for uncovering functionally-­
relevant components of the bat immune response to virus infection are needed. To address this need, we have 
developed  an  innovative  arbovirus  "rescue"  assay  wherein  immune  evasion  proteins  (IEPs)  encoded  by 
mammalian pathogens can be expressed in bat cells and one can assay for changes in bat cell susceptibility to 
arbovirus infection. Enhancement of arbovirus replication after expression of a candidate IEP indicates that the 
IEP  likely  inhibits  bat  immunity  mechanisms  that  normally  restrict  arbovirus  replication.  Using  these  IEPs  as 
"tools",  one  can  then  identify  the  bat  immunity  factors  these  IEPs  target.  Thus,  this  screening  methodology 
provides  a  mechanism  to  both  identify  novel  IEPs  and  functionally-­relevant  components  of  the  bat  immune 
response. To discover IEPs that promote arbovirus replication in bat cells, we will screen an expression library 
encoding ~200 bacterial effector proteins. Bacterial effectors are proteins secreted by pathogenic bacteria into 
eukaryotic  hosts  cells  that  modulate  or  inhibit  various  eukaryotic  cellular  processes  to  promote  bacterial 
replication.  Many  bacterial  pathogens  that  replicate  in the  cytoplasm  of  eukaryotic  host cells  encode  effectors 
that function as IEPs. Thus, we hypothesize that some effectors may suppress immune responses that restrict 
both  bacteria  and  cytoplasmic  viruses  such  as  arboviruses.  Indeed,  our  initial  screens  have  identified  four 
effectors  that  promote  the  replication  of  four  different  arboviruses  when  expressed  in  bat  cells.  We  have 
characterized one of these effector screen "hits" as a novel ubiquitin ligase that targets an uncharacterized Ring 
Finger (RNF) Domain-­containing protein for degradation in eukaryotic cells. Importantly, RNAi depletion of this 
RNF factor in human and bat cells promotes arbovirus replication, suggesting that it may be a novel component 
of human and bat immune responses. These results suggest that we can use bacterial effectors as tools to both 
inhibit, and identify, functionally-­relevant immunity factors in bats. Our study has the following specific aims: 1) 
Identify  bacterial  effector  proteins  that  promote  arbovirus  replication  in  bat  cells;;  2)  Identify  bat  proteins 
interacting  with  effector  “hits”  from  our  arbovirus  rescue  assays;;  and  3)  Determine  which  bat  host  factors 
interacting  with  effector  protein  hits  affect  viral  replication.  Our  long-­term  goal  is  to  use  this  model  system  to 
define the key bat innate immune mechanisms that restrict arbovirus replication.  
 
 
 
 

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