Body temperature of monkeys after NiV challenge.

<p>The rectal temperature of unimmunized (upper) monkeys or monkeys immunized with 10⁵ TCID₅₀ of rMV-Ed-G was recorded from 4 days before the NiV challenge until the end of the experiment. T+ B8144 and T+ SV085 were unimmunized monkeys. Ed B8358 and Ed B8192 were monkeys immunized with rMV-Ed-G before virus challenge.</p

Histopathology of monkey tissues.

<p>Lung and brain samples from unvaccinated monkeys (T +B8144, T+ SV085) and vaccinated monkeys (Ed B8358, Ed 8192) were stained with hematoxylin and eosin. 100× magnification. The lungs of T+ B8144 and T+ SV085 showed severe congestion, infiltration of neutrophils and accumulation of blood plasma in the alveoli. Their brains showed perivascular cuffing (black arrow; SV085) and an accumulation of glial (white arrow; SV 085) and foam cells (white arrow in; B8144) in the cerebral cortex. No lesions were observed in tissues from Ed B8358 or Ed B8192.</p

Pathological findings in organ samples of NiV infected monkeys.

<p>Pathological findings in organ samples of NiV infected monkeys.</p

Virus replication in Nipah virus-infected monkeys.

<p>Virus replication was determined in tissues (A) and oral and nasal swabs (B) of NiV-infected animals by qPCR. (A) Tissue samples of monkeys infected <i>via</i> the intraperitoneal (IP) route were collected at 7 dpi, while samples from monkeys infected <i>via</i> intranasal (IN)+per os (PO) route were collected at 24 dpi. (B) Nasal and pharynx swab samples were collected every 2 days. All samples were measured in triplicate, and error bars represent the standard error of the mean (SEM).</p

Vaccination with rMV-Ed-G induced well antibody responses in monkeys.

<p>Monkeys were immunized with rMV-Ed-G twice on d0 and d28. Antibody levels were measured by ELISA. Shadowed columns represent the samples which showed positive response. T+: unimmunized. ND: Not detected (<1∶100).</p

Recombinant measles virus expressing NiV G protein.

<p>Two strains of rMV expressing the NiV G protein were generated; rMV-HL-G and rMV-Ed-G. (A) rMV-HL-G-infected B95a cells and rMV-Ed-G-infected Vero cells were stained with anti-NiV G polyclonal antibody and analyzed by phase contrast microscopy and immunofluorescence. Cells infected with empty vectors served as controls. (B) B95a cells were infected with rMV-HL or rMV-HL-G. Vero cells were infected with rMV-Ed or rMV-Ed-G. Infections were conducted at a multiplicity of infection (MOI) of 0.1 TCID₅₀/cell. Cells and supernatants were collected at the indicated time points for determination of virus titer. Error bars indicate means ± the standard deviation (SD) from three experiments.</p

Body weights of Nipah virus-infected monkeys.

<p>Each monkey was inoculated with 10⁸ or 10⁶ TCID₅₀ of NiV <i>via</i> intraperitoneal (A) or intranasal and oral routes (B). Monkeys were examined every 2–3 days, and body weights recorded. Levels were standardized, with the weight at the first day of the experiment set as 1.</p

Survival curves of the hamsters infected with different quantities of the recombinant viruses.

<p>Hamsters (6 groups) were inoculated intraperitoneally with 10-fold serial dilutions of either NiV or rNiVs and survival rate of each group was observed for 30 days. (A) shows survival curves of hamsters infected with rNiV(W−) and (B) shows that of hamsters infected with rNiV(V−) and rNiV(C−).</p

Experimental Infection of Macaques with a Wild Water Bird-Derived Highly Pathogenic Avian Influenza Virus (H5N1)

<div><p>Highly pathogenic avian influenza virus (HPAIV) continues to threaten human health. Non-human primate infection models of human influenza are desired. To establish an animal infection model with more natural transmission and to determine the pathogenicity of HPAIV isolated from a wild water bird in primates, we administered a Japanese isolate of HPAIV (A/whooper swan/Hokkaido/1/2008, H5N1 clade 2.3.2.1) to rhesus and cynomolgus monkeys, in droplet form, via the intratracheal route. Infection of the lower and upper respiratory tracts and viral shedding were observed in both macaques. Inoculation of rhesus monkeys with higher doses of the isolate resulted in stronger clinical symptoms of influenza. Our results demonstrate that HPAIV isolated from a water bird in Japan is pathogenic in monkeys by experimental inoculation, and provide a new method for HPAIV infection of non-human primate hosts, a good animal model for investigation of HPAIV pathogenicity. </p> </div

Nipah P, V, W and C proteins inhibit IFN-signaling.

<p>293 cells were transfected with pISRE-luc, an internal control vector pRL-CMV and the indicated expression constructs (P, V, W or C) or empty vector (ctrl). At 36 h post transfection, the medium was changed to one containing 1 000 IU/ml of IFN-α. Luciferase assay was performed after 8 h incubation. All data were normalized by the expression level of <i>Renilla</i> luciferase, and the relative luciferase activity of the IFN-α treated (right shaded column) and untreated (left open column) cells is shown. The numbers at the top of the columns indicate the fold increase of luciferase activity upon IFN-α treatment. Error bars indicate the means ± the SD of three experiments.</p