Faculty Opinions recommendation of Emergence and pathogenicity of highly virulent Cryptococcus gattii genotypes in the northwest United States.

A recent outbreak of particularly virulent disease caused by porcine reproductive and respiratory syndrome virus has occurred in swine herds across the United States. We report here the complete genome sequence of eight viral isolates from four Nebraska herds experiencing an outbreak of severe disease in 2016.

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Cryptococcus gattii Infection Dampens Th1 and Th17 Responses by Attenuating Dendritic Cell Function and Pulmonary Chemokine Expression in the Immunocompetent Hosts

Infection and Immunity ◽

10.1128/iai.01773-14 ◽

2014 ◽

Vol 82 (9) ◽

pp. 3880-3890 ◽

Cited By ~ 35

Author(s):

Pornpimon Angkasekwinai ◽

Nuntarat Sringkarin ◽

Oratai Supasorn ◽

Madtika Fungkrajai ◽

Yui-Hsi Wang ◽

...

Keyword(s):

Immune Responses ◽

Cell Function ◽

Cryptococcus Gattii ◽

Cell Immune Response ◽

Content Type ◽

Chemokine Expression ◽

Immunocompromised Hosts ◽

The Impact ◽

Highly Virulent

ABSTRACTCryptococcal infections are primarily caused by two related fungal species:Cryptococcus neoformansandCryptococcus gattii. It is well known thatC. neoformansgenerally affects immunocompromised hosts; however,C. gattiiinfection can cause diseases in not only immunocompromised hosts but also immunocompetent individuals. While recent studies suggest thatC. gattiiinfection could dampen pulmonary neutrophil recruitment and inflammatory cytokine production in immunocompetent hosts, the impact ofC. gattiiinfection on the development of their adaptive T helper cell immune response has not been addressed. Here, we report thatC. neoformansinfection with highly virulent and less virulent strains preferentially induced pulmonary Th1 and Th17 immune responses in the host, respectively. However, fewer pulmonary Th1 and Th17 cells could be detected in mice infected withC. gattiistrains. Notably, dendritic cells (DC) in mice infected withC. gattiiexpressed much lower levels of surface MHC-II andIl12orIl23transcripts and failed to induce effective Th1 and Th17 differentiationin vitro. Furthermore, the expression levels ofIp10andCxcl9transcripts, encoding Th1-attracting chemokines, were significantly reduced in the lungs of mice infected with the highly virulentC. gattiistrain. Thus, our data suggest thatC. gattiiinfection dampens the DC-mediated effective Th1/Th17 immune responses and downregulates the pulmonary chemokine expression, thus resulting in the inability to mount protective immunity in immunocompetent hosts.

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Pyricularia grisea Causing Gray Leaf Spot of Perennial Ryegrass Turf: Population Structure and Host Specificity

Plant Disease ◽

10.1094/pdis.2001.85.8.817 ◽

2001 ◽

Vol 85 (8) ◽

pp. 817-826 ◽

Cited By ~ 38

Author(s):

G. Viji ◽

B. Wu ◽

S. Kang ◽

W. Uddin ◽

D. R. Huff

Keyword(s):

United States ◽

Population Structure ◽

Winter Wheat ◽

Perennial Ryegrass ◽

Leaf Spot ◽

Genetic Relationships ◽

The United States ◽

Gray Leaf Spot ◽

Pyricularia Grisea ◽

Highly Virulent

Gray leaf spot is a serious disease of perennial ryegrass (Lolium perenne) turf in the United States. Isolates of Pyricularia grisea causing the disease in perennial ryegrass were characterized using molecular markers and pathogenicity assays on various gramineous hosts. Genetic relationships among perennial ryegrass isolates were determined using different types of trans-posons as probes. Phylogenetic analysis using Pot2 and MGR586 probes, analyzed with AMOVA (analysis of molecular variance), showed that these isolates from perennial ryegrass consist of three closely related lineages. All the isolates belonged to a single mating type, MAT1-2. Among 20 isolates from 16 host species other than perennial ryegrass, only the isolates from wheat (Triticum aestivum) and triticale (× Triticosecale), showed notable similarity to the perennial ryegrass isolates based on their Pot2 fingerprints. The copy number and fingerprints of Pot2 and MGR586 in isolates of P. grisea from perennial ryegrass indicate that they are genetically distinct from the isolates derived from rice (Oryza sativa) in the United States. The perennial ryegrass isolates also had the same sequence in the internal transcribed spacer (ITS) region of the genes encoding ribosomal RNA as that of the wheat and triticale isolates, and exhibited rice isolate sequence polymorphisms. In pathogenicity assays, all the isolates of P. grisea from Legacy II perennial ryegrass caused characteristic blast symptoms on Marilee soft white winter wheat, Bennett hard red winter wheat, Era soft white spring wheat, and Presto triticale, and they were highly virulent on these hosts. An isolate from wheat and one from triticale (from Brazil) were also highly virulent on perennial ryegrass and Rebel III tall fescue (Festuca arundinacea). None of the isolates from perennial ryegrass caused the disease on Lagrue rice, and vice versa. Understanding the population structure of P. grisea isolates infecting perennial ryegrass and their relatedness to isolates from other gramineous hosts may aid in identifying alternate hosts for this pathogen.

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Phylogenetic Relationships among Highly Virulent Newcastle Disease Virus Isolates Obtained from Exotic Birds and Poultry from 1989 to 1996

Journal of Clinical Microbiology ◽

10.1128/jcm.36.4.1141-1145.1998 ◽

1998 ◽

Vol 36 (4) ◽

pp. 1141-1145 ◽

Cited By ~ 35

Author(s):

Bruce S. Seal ◽

Daniel J. King ◽

Devin P. Locke ◽

Dennis A. Senne ◽

Mark W. Jackwood

Keyword(s):

United States ◽

Fusion Protein ◽

Newcastle Disease ◽

Cleavage Site ◽

The United States ◽

Protein Cleavage ◽

Exotic Birds ◽

Fusion Protein Cleavage Site ◽

Highly Virulent ◽

Fusion Protein Cleavage

Newcastle disease virus {NDV (avian paramyxovirus type 1 [APMV1])} isolates were recovered from imported exotic birds confiscated following importation into the United States, from waterbirds in the United States, and from poultry. The exotic birds probably originated from Central and South America, Asia, and Africa. The NDV isolates were initially characterized as highly virulent because of a short mean death time in embryonated chicken eggs. The isolates were typed as neurotropic or viscerotropic velogenic by intracloacal inoculation of adult chickens. Intracerebral pathogenicity index values for the virulent NDV isolates ranged from 1.54 to 1.90, compared to a possible maximum value of 2.0. These isolates had a dibasic amino acid motif in the fusion protein cleavage site sequence required for host systemic replication. Sequence differences were detected surrounding the fusion protein cleavage site and the matrix protein nuclear localization signal, indicating evolution of highly virulent NDV. Phylogenetically, these isolates were categorized with other highly virulent NDV strains that caused outbreaks in southern California poultry during 1972 and in cormorants in the north central United States and southern Canada during 1990 and 1992. These isolates are related to NDV that may have the APMV1 strain chicken/Australia/AV/32 or a related virus as a possible progenitor. Recent virulent NDV isolates and those recovered during disease outbreaks since the 1970s are phylogenetically distinct from current vaccine viruses and standard challenge strains.

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