Rhadinovirus Host Entry by Co-operative Infection
All viral infections start with host entry. Entry into cells is studied widely in isolated cultures; entry into live hosts is more complicated and less well understood: our tissues have specific anatomical structures and our cells differ markedly from most cultured cells in size, shape and behaviour. The respiratory tract is a common site of virus infection. Size dictates where inhaled particles come to rest, and virus-sized particles can reach the lungs. Rhadinoviruses chronically infect both humans and economically important animals, and cause lung disease. We used a well-characterized murine example to determine how a rhadinovirus enters the lungs. At its peak, infection was prominent in epithelial cells lining the lung air spaces. However it started in macrophages, which normally clear the lungs of inhaled debris. Only epithelial cells expressed the molecules required for virus binding, but only macrophages internalized virus particles after binding; infection involved interaction between these different cell types. Blocking epithelial infection with an antibody did not stop host entry because attached antibodies increase virus uptake by lung macrophages; but an antibody that blocks macrophage infection was effective. Thus, understanding how rhadinovirus infections work in normal tissues provided important information for their control.
Vyšlo v časopise:
Rhadinovirus Host Entry by Co-operative Infection. PLoS Pathog 11(3): e32767. doi:10.1371/journal.ppat.1004761
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1004761
Souhrn
All viral infections start with host entry. Entry into cells is studied widely in isolated cultures; entry into live hosts is more complicated and less well understood: our tissues have specific anatomical structures and our cells differ markedly from most cultured cells in size, shape and behaviour. The respiratory tract is a common site of virus infection. Size dictates where inhaled particles come to rest, and virus-sized particles can reach the lungs. Rhadinoviruses chronically infect both humans and economically important animals, and cause lung disease. We used a well-characterized murine example to determine how a rhadinovirus enters the lungs. At its peak, infection was prominent in epithelial cells lining the lung air spaces. However it started in macrophages, which normally clear the lungs of inhaled debris. Only epithelial cells expressed the molecules required for virus binding, but only macrophages internalized virus particles after binding; infection involved interaction between these different cell types. Blocking epithelial infection with an antibody did not stop host entry because attached antibodies increase virus uptake by lung macrophages; but an antibody that blocks macrophage infection was effective. Thus, understanding how rhadinovirus infections work in normal tissues provided important information for their control.
Zdroje
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Hygiena a epidemiológia Infekčné lekárstvo LaboratóriumČlánok vyšiel v časopise
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