Avian Influenza A(H7N2) Virus in Human Exposed to Sick Cats, New York, USA, 2016.

An outbreak of influenza A(H7N2) virus in cats in a shelter in New York, NY, USA, resulted in zoonotic transmission. Virus isolated from the infected human was closely related to virus isolated from a cat; both were related to low pathogenicity avian influenza A(H7N2) viruses detected in the United States during the early 2000s.

First Detection of Avian Lineage H7N2 in .

In December 2016, influenza A (H7N2) was first detected among cats in the New York City shelter system with subsequent widespread transmission. The sequence of the first clinical isolate, A/feline/New York/16-040082-1/2016(H7N2), and its genetic similarity to the live bird market lineage of H7N2 low-pathogenicity avian influenza are described.

Prolonged intermittent virus shedding during an outbreak of canine influenza A H3N2 virus infection in dogs in three Chicago area shelters: 16 cases (March to May 2015).

OBJECTIVE To estimate an appropriate isolation period for dogs infected with canine influenza A H3N2 virus on the basis of the duration of virus shedding. DESIGN Retrospective case series. ANIMALS 16 dogs, from 3 Chicago area shelters, naturally infected with canine influenza A H3N2 virus.

Beak necrosis in Hungarian partridges (Perdix perdix) associated with beak-bits and avian poxvirus infection.

Proliferative growth, consistent with poxvirus infection, encapsulated plastic beak-bits and covered the dorsal portion of the upper beak and nares of adult male and female captive-raised Hungarian partridges. Three representative birds were submitted to the Wisconsin Veterinary Diagnostic Laboratory for necropsy. Lesions in the necropsied birds extended through the nares, where the plastic bit ends are designed to rest.

Encephalitis in aborted bovine fetuses associated with Bovine herpesvirus 1 infection.

Brain tissue from 12 aborted bovine fetuses submitted to the Wisconsin Veterinary Diagnostic Laboratory revealed histologic lesions that consisted of glial nodules and variable degrees of mononuclear inflammation, microhemorrhage, neuronal necrosis, and cerebral cortical cavitation. A diagnosis of Bovine herpesvirus 1 (BHV-1) abortion had been made in all of these cases through multiple testing modalities. Brain tissue from 8 of the 12 fetuses was immunohistochemically stained with a monoclonal antibody specific to BHV-1, and, in 5 fetuses, there was positive intralesional staining of neurons, glial cells, and endothelial cells.

Plasmodium chabaudi adami: interferon-gamma but not IL-2 is essential for the expression of cell-mediated immunity against blood-stage parasites in mice.

Cell-mediated immunity (CMI) may be important in immunity against blood-stage malaria. Accordingly, we examined the role of type 1 cytokines in the resolution of Plasmodium chabaudi adami malaria in mice genetically modified to have type 1 cytokine gene defects. Parasitemia was prolonged in double knockout (IL-2(-/-), IFNgamma(-/-)) mice compared to control mice.

Immunity to blood-stage murine malarial parasites is MHC class II dependent.

To determine whether MHC class II antigen presentation is essential for the induction of protective immunity against blood-stage malarial parasites, we used gene-targeted knockout (KO) mice to follow the time-course of nonlethal Plasmodium yoelii and Plasmodium chabaudi infections in two models of MHC class II deficiency. Infection of MHC class II KO (A(-/-)) mice with either parasite species resulted in an unremitting hyperparasitemia, whereas MHC-intact control mice resolved their parasitemia. In contrast, invariant chain KO (Ii(-/-)) mice, which present antigen via recycled but not nascent MHC class II molecules, eventually cured their infections when infected with P.

Plasticity of immune responses suppressing parasitemia during acute Plasmodium chabaudi malaria.

gammadelta T cells have a crucial role in cell-mediated immunity (CMI) against P. chabaudi malaria, but delta-chain knockout (KO) (deltao/o) mice and mice depleted of gammadelta T cells with mAb cure this infection. To address the question of why mice deficient in gammadelta T cells resolve P.

The time course of selected malarial infections in cytokine-deficient mice.

Murine malarial parasites have long been characterized by their requirement for either antibody-mediated immunity (AMI) or cell-mediated immunity (CMI) for suppression of acute parasitemia, with Plasmodium yoelii reportedly requiring AMI for suppression and P. chabaudi requiring CMI. To assess this characterization in terms of the current T(H1)/T(H2)-CMI/AMI hypothesis, we infected gene-targeted "knockout" mice lacking either a type-1 cytokine (IL-2 or IFN-gamma) or a type-2 cytokine (IL-4 or IL-10) with one or the other species of Plasmodium.

Increased gamma-delta T-lymphocyte response to Mycobacterium bovis BCG in major histocompatibility complex class I-deficient mice.

Mice with a homologous deletion of the beta 2-microglobulin gene (beta 2m-) are deficient in class I major histocompatibility complex molecules (MHC) and consequently are deficient in CD8+ T cells. These beta 2m- mutant mice control the intraperitoneal growth of an avirulent vaccine strain of mycobacteria, Mycobacterium bovis BCG, after intraperitoneal infection similarly to normal mice. We show that beta 2m- mice have an increased gamma-delta (gamma delta) T-cell response after infection with live avirulent mycobacteria.

Human T cells in hu-PBL-SCID mice proliferate in response to Daudi lymphoma and confer anti-tumour immunity.

In vitro culture of human peripheral blood lymphocytes (PBL) with Daudi (Burkitt lymphoma) cells results in selective proliferation of V gamma 9/V delta 2 T cells with high cytotoxicity against Daudi cells. After adoptive transfer into severe combined immunodeficient (SCID) mice, these cells exert specific anti-tumour activity against Daudi lymphoma. To test whether cytotoxic V gamma 9/V delta 2 T cells are induced in SCID mice, human PBL injected intraperitoneally were stimulated with irradiated Daudi cells (PBL/Daudi-SCID).

In vitro preactivated human T cells engraft in SCID mice and migrate to murine lymphoid tissues.

Mice with severe combined immunodeficiency (SCID) accept grafts of human T and B lymphocytes derived from resting peripheral blood mononuclear cells (PBMC). We wished to determine whether activated human T cells engraft and migrate into lymphoid tissues in SCID mice. PBMC (50 x 10(6)) activated in vitro in a 4-day mixed lymphocyte culture (MLC) were injected into the peritoneum of 12 SCID mice.

Antilymphoma activity of human gamma delta T-cells in mice with severe combined immune deficiency.

Human Burkitt lymphoma (Daudi) cells grow as disseminated tumors in mice with severe combined immune deficiency (SCID) after either i.v. or i.