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HMPV Impairs Macrophage Phagocytosis Through a Replication-Dependent Mechanism Associated with Reduced CD36

Iván Martínez-Espinoza1, Pius I Babawale1, Basel Abuaita1

  • 1Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.

Viruses
|June 26, 2026
PubMed

Insights

Human metapneumovirus (HMPV) impairs macrophage bacterial uptake via a cell-intrinsic mechanism. This involves reduced scavenger receptor CD36 expression, potentially increasing secondary infection risk.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Macrophages are critical for host defense against bacterial infections via phagocytosis.
  • Human metapneumovirus (HMPV) is a significant respiratory pathogen, but its effects on macrophage function are unclear.
  • Impaired macrophage phagocytosis can lead to increased susceptibility to secondary bacterial infections.

Purpose of the Study:

  • To investigate the impact of HMPV infection on macrophage antibacterial functions.
  • To elucidate the mechanisms by which HMPV affects phagocytosis.
  • To identify viral factors involved in HMPV-induced immune dysfunction.

Main Methods:

  • Infection of THP-1 derived macrophages with HMPV.
  • Assessment of bacterial uptake and phagocytosis.
  • Analysis of scavenger receptor CD36 expression.
  • Viral gene knockdown studies (HMPV G protein).
  • Analysis of single-cell RNA-sequencing data from HMPV-infected mouse lungs.
  • Gene expression analysis (Cd36, Marco) in mouse lung tissue.

Main Results:

  • HMPV infection significantly reduced bacterial uptake in macrophages in a replication-dependent manner.
  • The impairment of phagocytosis was a cell-intrinsic effect, restricted to infected cells.
  • HMPV infection led to reduced expression of the scavenger receptor CD36.
  • Knockdown of the HMPV G protein restored macrophage phagocytic function.
  • Analysis of mouse lung data showed reduced CD36 expression and altered phagocytosis-associated gene programs in lung macrophages.

Conclusions:

  • HMPV infection impairs macrophage bacterial uptake through a replication-dependent, cell-intrinsic mechanism.
  • Reduced scavenger receptor expression (CD36) and the viral G protein are key factors in HMPV-induced phagocytic dysfunction.
  • These HMPV-induced alterations in macrophage function may increase the risk of secondary bacterial infections.
Keywords:
CD36HMPVhuman metapneumovirusphagocytosisrespiratoryvirus

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