Severe and Persistent Depletion of Circulating Plasmacytoid Dendritic Cells in Patients with 2009 Pandemic H1N1 Infection
2011

Depletion of Dendritic Cells in H1N1 Infection

Sample size: 13 publication Evidence: moderate

Author Information

Author(s): Lichtner Miriam, Mastroianni Claudio M., Rossi Raffaella, Russo Gianluca, Belvisi Valeria, Marocco Raffaella, Mascia Claudia, Del Borgo Cosmo, Mengoni Fabio, Sauzullo Ilaria, d'Ettorre Gabriella, D'Agostino Claudia, Massetti Anna P., Vullo Vincenzo

Primary Institution: Sapienza University

Hypothesis

The study aims to evaluate the pattern of innate immune response during human 2009 H1N1 infection.

Conclusion

H1N1 disease is associated with a profound depletion of dendritic cell subsets, particularly plasmacytoid dendritic cells, which do not fully recover even after several weeks.

Supporting Evidence

  • H1N1-infected patients exhibited a significant depletion in both circulating plasmacytoid and myeloid dendritic cells.
  • Patients showed a decrease in CD4 and CD8 T cell counts during the acute phase of the disease.
  • Plasmatic hyperproduction of IP-10 and RANTES was observed in H1N1-infected patients.
  • Patients did not achieve a complete recovery of plasmacytoid dendritic cell counts even after 16 weeks.

Takeaway

When people get sick from the H1N1 flu, their bodies lose important immune cells called dendritic cells, which help fight infections. Even after they feel better, some of these cells don't come back to normal levels.

Methodology

Blood samples were collected from 13 hospitalized patients with confirmed H1N1 pneumonia at admission and during follow-up at weeks 1, 4, and 16.

Limitations

The study did not analyze viral load kinetics and included only patients with confirmed influenza pneumonia.

Participant Demographics

Among the 13 enrolled patients, 6 were males and 7 females, with a median age of 44 years.

Statistical Information

P-Value

p<0.001

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0019872

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