Patrick C. Reading

Vaccinia virus CrmE encodes a soluble and cell surface tumor necrosis factor receptor that contributes to virus virulence.

Dermal infection with vaccinia virus reveals roles for virus proteins not seen using other inoculation routes.

The vaccinia virus C12L protein inhibits mouse IL-18 and promotes virus virulence in the murine intranasal model.

A soluble chemokine-binding protein from vaccinia virus reduces virus virulence and the inflammatory response to infection.

The poxvirus protein A52R targets Toll-like receptor signaling complexes to suppress host defense.

Steroid hormone synthesis by vaccinia virus suppresses the inflammatory response to infection.

A kinetic analysis of immune mediators in the lungs of mice infected with vaccinia virus and comparison with intradermal infection.

The vaccinia virus kelch-like protein C2L affects calcium-independent adhesion to the extracellular matrix and inflammation in a murine intradermal model.

Vaccinia virus interleukin-18-binding protein promotes virulence by reducing gamma interferon production and natural killer and T-cell activity.

Vaccinia virus protein A46R targets multiple Toll-like-interleukin-1 receptor adaptors and contributes to virulence.

NK cells contribute to the early clearance of HSV-1 from the lung but cannot control replication in the central nervous system following intranasal infection.

A role for plasmacytoid dendritic cells in the rapid IL-18-dependent activation of NK cells following HSV-1 infection.

IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection.

Glycosylation as a target for recognition of influenza viruses by the innate immune system.

Antiviral activity of the long chain pentraxin PTX3 against influenza viruses.

The role of neutrophils in the upper and lower respiratory tract during influenza virus infection of mice.

Memory T cells in nonlymphoid tissue that provide enhanced local immunity during infection with herpes simplex virus.

Neutrophils ameliorate lung injury and the development of severe disease during influenza infection.

Loss of a single N-linked glycan from the hemagglutinin of influenza virus is associated with resistance to collectins and increased virulence in mice.

Macrophage receptors for influenza A virus: role of the macrophage galactose-type lectin and mannose receptor in viral entry.

Influenza viruses differ in ability to infect macrophages and to induce a local inflammatory response following intraperitoneal injection of mice.

Critical role of airway macrophages in modulating disease severity during influenza virus infection of mice.

Depletion of Gr-1+, but not Ly6G+, immune cells exacerbates virus replication and disease in an intranasal model of herpes simplex virus type 1 infection.

Gr-1+ cells, but not neutrophils, limit virus replication and lesion development following flank infection of mice with herpes simplex virus type-1.

Pandemic H1N1 influenza A viruses are resistant to the antiviral activities of innate immune proteins of the collectin and pentraxin superfamilies.

Inhibition of lectin-mediated innate host defences in vivo modulates disease severity during influenza virus infection.

Correlation between sialic acid expression and infection of murine macrophages by different strains of influenza virus.

N-linked glycosylation facilitates sialic acid-independent attachment and entry of influenza A viruses into cells expressing DC-SIGN or L-SIGN.

Glycosylation of the hemagglutinin modulates the sensitivity of H3N2 influenza viruses to innate proteins in airway secretions and virulence in mice.

Receptor specificity of the influenza virus hemagglutinin modulates sensitivity to soluble collectins of the innate immune system and virulence in mice.

The role of neutrophils during mild and severe influenza virus infections of mice.

Responses of mouse airway epithelial cells and alveolar macrophages to virulent and avirulent strains of influenza A virus.

Neutrophils sustain effective CD8(+) T-cell responses in the respiratory tract following influenza infection.

Specific sites of N-linked glycosylation on the hemagglutinin of H1N1 subtype influenza A virus determine sensitivity to inhibitors of the innate immune system and virulence in mice.

Influenza virus induces bacterial and nonbacterial otitis media.

Cell-surface receptors on macrophages and dendritic cells for attachment and entry of influenza virus.