Tropism of SARS-CoV-2 for human cortical astrocytes. Andrews, M. G, Mukhtar, T., Eze, U. C, Simoneau, C. R, Ross, J., Parikshak, N., Wang, S., Zhou, L., Koontz, M., Velmeshev, D., Siebert, C., Gemenes, K. M, Tabata, T., Perez, Y., Wang, L., Mostajo-Radji, M. A, de Majo, M., Donohue, K. C, Shin, D., Salma, J., Pollen, A. A, Nowakowski, T. J, Ullian, E., Kumar, G R., Winkler, E. A, Crouch, E. E, Ott, M., & Kriegstein, A. R Proc Natl Acad Sci U S A, 119(30):e2122236119, July, 2022.
abstract   bibtex   
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) readily infects a variety of cell types impacting the function of vital organ systems, with particularly severe impact on respiratory function. Neurological symptoms, which range in severity, accompany as many as one-third of COVID-19 cases, indicating a potential vulnerability of neural cell types. To assess whether human cortical cells can be directly infected by SARS-CoV-2, we utilized stem-cell-derived cortical organoids as well as primary human cortical tissue, both from developmental and adult stages. We find significant and predominant infection in cortical astrocytes in both primary tissue and organoid cultures, with minimal infection of other cortical populations. Infected and bystander astrocytes have a corresponding increase in inflammatory gene expression, reactivity characteristics, increased cytokine and growth factor signaling, and cellular stress. Although human cortical cells, particularly astrocytes, have no observable ACE2 expression, we find high levels of coronavirus coreceptors in infected astrocytes, including CD147 and DPP4. Decreasing coreceptor abundance and activity reduces overall infection rate, and increasing expression is sufficient to promote infection. Thus, we find tropism of SARS-CoV-2 for human astrocytes resulting in inflammatory gliosis-type injury that is dependent on coronavirus coreceptors.
@ARTICLE{Andrews2022-ty,
  title    = "Tropism of {SARS-CoV-2} for human cortical astrocytes",
  author   = "Andrews, Madeline G and Mukhtar, Tanzila and Eze, Ugomma C and
              Simoneau, Camille R and Ross, Jayden and Parikshak, Neelroop and
              Wang, Shaohui and Zhou, Li and Koontz, Mark and Velmeshev, Dmitry
              and Siebert, Clara-Vita and Gemenes, Kaila M and Tabata, Takako
              and Perez, Yonatan and Wang, Li and Mostajo-Radji, Mohammed A and
              de Majo, Martina and Donohue, Kevin C and Shin, David and Salma,
              Jahan and Pollen, Alex A and Nowakowski, Tomasz J and Ullian,
              Erik and Kumar, G Renuka and Winkler, Ethan A and Crouch,
              Elizabeth E and Ott, Melanie and Kriegstein, Arnold R",
  abstract = "The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
              readily infects a variety of cell types impacting the function of
              vital organ systems, with particularly severe impact on
              respiratory function. Neurological symptoms, which range in
              severity, accompany as many as one-third of COVID-19 cases,
              indicating a potential vulnerability of neural cell types. To
              assess whether human cortical cells can be directly infected by
              SARS-CoV-2, we utilized stem-cell-derived cortical organoids as
              well as primary human cortical tissue, both from developmental
              and adult stages. We find significant and predominant infection
              in cortical astrocytes in both primary tissue and organoid
              cultures, with minimal infection of other cortical populations.
              Infected and bystander astrocytes have a corresponding increase
              in inflammatory gene expression, reactivity characteristics,
              increased cytokine and growth factor signaling, and cellular
              stress. Although human cortical cells, particularly astrocytes,
              have no observable ACE2 expression, we find high levels of
              coronavirus coreceptors in infected astrocytes, including CD147
              and DPP4. Decreasing coreceptor abundance and activity reduces
              overall infection rate, and increasing expression is sufficient
              to promote infection. Thus, we find tropism of SARS-CoV-2 for
              human astrocytes resulting in inflammatory gliosis-type injury
              that is dependent on coronavirus coreceptors.",
  journal  = "Proc Natl Acad Sci U S A",
  volume   =  119,
  number   =  30,
  pages    = "e2122236119",
  month    =  jul,
  year     =  2022,
  keywords = "SARS-CoV-2 tropism; astrocyte reactivity; organoid models",
  language = "en"
}
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