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Q I’ve already blown off my New Year’s vow to lose weight. Can I still reach my goal by summer?

A Absolutely! You’re not alone–36 percent of us have already strayed from our yearly get-healthy objectives, finds a study from the University of Scranton. But with a few tweaks, say experts, you can jump back on the weight-loss wagon.

What distinguishes a resolution-maker from a resolution-breaker is having a specific, attainable goal. "Many women tend to set pie-in-the-sky targets, like losing 15 pounds in a month," says Keri M. Gans, R.D., a New York City nutritionist and spokeswoman for the American Dietetic Association. "Trying to do too much too fast can cause you to become frustrated and give up."

Gans suggests rewording your objective so it focuses on behaviors you can change rather than on an arbitrary number on the scale. "Break down your overall goal into smaller, more manageable ones, emphasizing what you’re adding to your diet rather than what you’re giving up," she says. Tackle a few easy items on your list first, like doing five push-ups every morning or switching to leaner cuts of meat. Pledge to sneak fruit into every dessert, or swap sorbet for ice cream. Once you’ve mastered those changes, try more challenging ones, like packing your lunch instead of hitting the deli or taking a kickboxing class after work.

Q A friend told me there’s a virus that can make you fat. Is this true?

A Right now, it’s just a theory. However, some researchers are so convinced Human adenovirus-36 (Ad-36) may be partly to blame for obesity, they’re developing medications to counteract its effects. "Lab experiments suggest this virus has the power to turn adult stem cells into fat cells," says Richard L. Atkinson, M.D., director of the Obetech Obesity Research Center. A study he published in the International Journal of Obesity found that people who tested positive for Ad-36 had a BMI 9 points higher than those who didn’t have the virus. Obese people were also about three times more likely to have been infected than their slimmer counterparts.

The good news: If you’re at a healthy weight now, you probably don’t need to worry about contracting Ad-36. "After being exposed to similar viruses that cause colds, flus, and illnesses, most adults have developed antibodies that protect them against catching it," says Atkinson.

Also, keep in mind that even if science can prove this virus directly leads to extra pounds, Atkinson says it probably affects only 10 to 20 percent of the population. "Lack of exercise, poor eating habits, and genetics are still the most common factors leading to weight gain," he says.

HAVE A WEIGHT-LOSS QUESTION? Write Shape, Weight-Loss Q & A, 1 Park Ave., 10th floor, New York, NY 10016 or weightlossq&a@shape.com.

COPYRIGHT 2008 Weider Publications
COPYRIGHT 2008 Gale, Cengage Learning

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[ILLUSTRATION OMITTED]

There isn’t a day that goes by that Michelle Villers doesn’t think of–or talk about–her daughter, Airman Paige Villers.

She can’t help it. Because when she talks about her Paige, whom she lovingly calls her Yellow Rose, a smile lights up Michelle’s face. Then she gets that far-away look in her eyes.

That’s when the words start pouring out, like the tears that will certainly follow.

Michelle is quick, almost anxious, to talk about Paige. Like she doesn’t want anyone to forget her or what she accomplished during her young life.

She recounts how Paige was born in Dallas and was "the perfect little girl" growing up. She said Paige was quiet, yet fiercely independent. Silly but mature. She had many jobs, but never missed a day of work. And that though cleaning her room wasn’t a priority, standing up for what she thought was right was. Michelle knew her daughter loved helping others, but didn’t know what color her hair would be the next week.

"My daughter made mistakes," Michelle said. "But she tried to make things right."

[ILLUSTRATIONS OMITTED]

Duty calls

But it’s when Michelle talks about Paige’s battle with the virus that cut short her Air Force career that emotion overwhelms her.

"Paige was so patriotic," Michelle said. "She loved everything about being in the Air Force."

That’s because behind Paige’s typical teenager’s facade, a restless young woman yearned for more than what rural Norton, Ohio, could offer. She dreamed of leaving her secure, small-town existence and starting her own life. The Air Force would let her do that, her mother said.

"She was so headstrong, yet so determined in everything she did," Michelle said. "When she set her mind to doing something–that was it–she was doing that no matter what happened."

A day after graduating from Norton High School, Paige told her mother and father, Don, she was joining the Air Force. She’d hinted at that before. Still, the Villers were surprised, and a bit apprehensive, about her joining the military during wartime. They asked her to think it over.

But Paige had made up her mind the Air Force she knew so little about was the right path to the new life she sought. There was no dissuading her, Michelle said.

So she went with her father to see Master Sgt. Sam Hensley, an Air Force recruiter. His office is in a strip mall at the end of Paige Avenue in Barberton, Ohio. Paige tried to learn all she could about the Air Force before visiting him in September 2006. She asked many questions and the interview went well, he said.

"She was determined to be in the Air Force from the moment she stepped into my office," said the sergeant, an 18-year air transportation veteran. "She made it very clear she wanted to serve her country, something you don’t typically see in an 18- or 19-year-old today."

Paige joined, and after a few months of waiting, packed her bag and headed for basic training at Lackland Air Force Base, Texas, in March 2007.

She started to live her dream.

"Paige was so excited. She joined the Air Force for honor, family and to finish her education," Michelle said, clutching a photograph of Paige tightly to her chest.

The photo shows a bright-eyed Paige in her light blue Air Force uniform shirt, a dark blue jacket and flight cap. She looks no older than 17–beaming with a smile of confidence.

Michelle tears up each time she looks at the photo.

"Paige looks so beautiful in her uniform," Michelle said. "I remember the day she had the picture taken. She called and said, ‘Mom, I got to put on my blues today. I feel so proud, so proud to be in the Air Force–so proud of this country.’"

Michelle recalls Paige’s previous calls home. On her first call, she sounded rushed and scared. But by about her third call home, Michelle could notice a change in her daughter.

"She sounded so sure of herself, so confident and mature–so happy," Michelle said.

Paige talked about basic training, her new life, friends and the sense of family she was experiencing. About being able to do the push-ups she couldn’t do before she left home. And about how she couldn’t wait to finish her training and start her Air Force career.

Christina Henry, Paige’s aunt, had never known her niece to be so joyful and excited.

"Paige wanted a life of honor, to do something that made a difference," Mrs. Henry said.

But Paige only got to realize part of her dream. She never got the chance to leave Lackland to start what she hoped would be a 20-year Air Force career of helping others.

The virus</p>

She started feeling sick during her fifth week of basic training, known as "Warrior Week." The weeklong exercise readies Airmen for deployment and living in field conditions.

"Paige loved Warrior Week. She said it rained a lot and it was muddy," Michelle said. "But she said it was awesome sleeping in a tent and experiencing the camaraderie."

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West Nile virus (WNV) was detected in the United States in 1999, has reoccurred every summer since, and has become endemic. Transfusion transmission was documented in 2002, and screening of blood donations for WNV began in 2003. We investigated genetic variation of WNV in human isolates obtained from specimens collected from 30 infected blood donors who tested positive for WNV RNA during 2002-2005. Complete genomic sequences of 8 isolates and structural gene sequences from 22 additional isolates were analyzed. We found some genetic diversity in isolates from different geographic regions and genetic divergence from reported sequences from epidemics in 1999-2001. Nucleotide divergence of structural genes showed a small increase from 2002 (0.18%) to 2005 (0.37%), suggesting absence of strong selective pressure and limited genetic evolution of WNV during that period. Nevertheless, WNV has continued to diverge from precursor isolates as geographic distribution of the virus has expanded.

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West Nile virus (WNV) is a small, enveloped, positive-strand RNA virus of the genus Flavivirus and a member of the Japanese encephalitis serocomplex. The plus-sense RNA genome is [approximately equal to] 11 kb and contains a single open reading frame flanked by 5′ and 3′ untranslated regions (UTRs). The encoded polyprotein is processed into 3 structural and 7 nonstructural (NS) proteins that are essential for viral replication, assembly, and release. WNV is maintained in nature by transmission between mosquitoes and birds but can also infect humans and other mammals (1) and reptiles (2). Most human infections are asymptomatic (70%-80%); symptomatic cases range from flulike illness to severe neurologic disease (>1% of cases) (3-5).

The first US outbreak of WNV occurred in 1999 in New York City; 68 human infections, mostly as meningoencephalitis, were confirmed, resulting in 7 deaths. Since 1999, WNV epidemics have reoccurred yearly with 23,975 reported human cases of disease and 962 deaths through 2006 (www.cdc.gov/ncidod/dvbid/westnile).

In 2002, the virus spread westward and the number of reported human cases increased dramatically. The North American epidemics of 2002 and 2003 represent the largest WNV outbreaks ever reported (6). Additional modes of WNV transmission were identified in 2002, including human-to-human transmissions from mother to child, organ transplantation, and blood transfusion (7-9). The quick spread of the virus raised questions regarding viral adaptation and prompted a detailed investigation of the genetic evolution of the virus.

The prototype WNV isolate, NY99-flamingo382-99 (WN-NY99; GenBank accession no. AF196835) was obtained from a flamingo infected during the 1999 outbreak in New York. This isolate belongs to lineage I and is most closely related to the Israel-98 goose isolate AF481864 (IS-98) (6,10). Phylogenetic comparisons of partial and complete nucleotide sequences from US isolates collected between the 1999 and 2000 epidemics with WN-NY99 isolate showed a high degree of genetic similarity with >99.8% nucleotide homology and >99.9% amino acid homology (11-14). A study of 22 different WNV isolates from 2001 and 2002 showed genetic variation of 0.35% (mean 0.18%) in the premembrane (preM) and envelope (env) genes compared with WN-NY99 (15).

Subsequently, 2 distinct genotypes were detected in strains obtained from Texas in 2002 (15). One new genetic variant widely spread over the United States diverged from the original WN-NY99 strain by several conserved nucleotide mutations and 1 aa substitution in the env protein. Recent studies have highlighted the emergence of a new WNV dominant genotype, named WN02, which has been increasingly prevalent in the United States since 2002 (16-19). Although 13 nt mutations became fixed in the new dominant genotype compared with the WN-NY99 prototype, the highest nucleotide sequence divergence of WNV strains isolated after 2002 is still in the range of 0.4%-0.5% (18,20). The reason for displacement of the WN-NY99 genotype by a new dominant genotype in North America is not clear, but could have been caused by differences in transmission efficiency of domestic mosquitoes that may offer a selective advantage for the newly emerged genotype (20,21).

Several studies on the genetic variation of WNV have been published (12,15,17,19,21,22). However, continuous monitoring of variability is needed because sensitivity of blood donor screening and diagnostic assays may be affected, producing a negative effect on public health. Genetic variability could also affect viral pathogenesis, development of vaccines, and development of efficacious therapeutic agents.

This study reports the genomic variation of WNV observed in clinical isolates obtained in the continental United States during 4 consecutive years (2002-2005). We observed an increase in the number of mutations in the full WNV genome from 0.18% in 2002 to 0.37% in 2005. It should be noted that 80% of the nucleotide changes in structural regions are transitions (T [left and right arrow] C) and 75% are silent mutations. Thus, WNV has continued to slowly diverge from precursor isolates as geographic distribution of the virus expanded.

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During the 2006-2007 winter season in South Korea, several outbreaks of highly pathogenic avian influenza virus (H5N1) were confirmed among domestic poultry and in migratory bird habitats. Phylogenetic analysis showed that all isolates were closely related and that all belong to the A/ bar-headed goose/Qinghai/5/2005-like lineage rather than the A/chicken/Korea/ES/2003–like lineage.

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Highly pathogenic avian influenza (HPAI) virus (H5N1) has been detected repeatedly in domestic poultry and wild birds since 1997, and it poses a substantial threat to human health (1,2). Since the end of 2003, influenza virus (HhN1) strains have spread in an unprecedented manner in many Asian countries, and the outbreaks have resulted in >170 human deaths in Thailand, Vietnam, Cambodia, and Indonesia. These outbreaks have also caused serious economic losses in the poultry industry (www.oie.int), including South Korea in 2003–the first official report of subtype H5N1 in South Korea’s history (3).

Since the outbreak caused by subtype H5N1 from migratory waterfowl on Qinghai Lake (QH) in May 2005 (4,5), outbreaks of QH-like avian influenza virus (H5N1) have been reported in the People’s Republic of China, Mongolia, Russia, Europe, and Africa, and have been ascribed to the migration of wild birds (6,7). In contrast to virus found in countries on the western side of Qinghai Lake, the Fujian-like avian influenza virus (H5N1) sublineage has predominated in southern China since late 2005 (8), but no outbreaks were reported in Far-Eastern Asian countries such as South Korea and Japan until October 2006. Eventually, in November 2006 and January 2007, outbreaks of HPAI (H5N1) occurred in South Korea and Japan. Here we report the second outbreak of HPAI (HhN1) among poultry in South Korea since November 2006 and its relationship with 2 HPAI virus (H5N1) strains isolated from migratory bird habitats (i.e., in the environment).

The Study

All of the virus strains from domestic poultry used in this study were isolated by the Korean National Veterinary Research and Quarantine Service (NVRQS) in embryonated eggs that were inoculated with tissues and swab specimens collected from the oropharynx and cloaca of affected birds. Two subtype H5N1 strains were isolated in embryonated eggs that had been inoculated with fecal specimens obtained from migratory bird habitats by Chungbuk National University and Chungnam National University. Viral genes were sequenced and analyzed as described (9). The full-length sequences for each segment were used in phylogenetic analyses. Gene sequences determined in this study have been deposited in GenBank under accession nos. EU233675-EU233746.

On November 22, 2006, NVRQS confirmed the first case of HPAI (HhN1) at a chicken farm in Iksan, Jeollabuk-Do, in South Korea. The affected flock contained 6,500 chickens and had shown a sudden increase in severe clinical signs and high mortality rate (86%), as reported by farmers and veterinarians (Table). During intensive surveillance in December 2006 within a 10-km radius (the surveillance zone) from the first outbreak farms, we found other HPAI (H5N1)–affected farms at Iksan (chicken farm, 3.4% deaths) and Gimje (quail farm, 4% deaths), Jeollabuk-Do (Figure 1).

On December 21, 2006, the fourth outbreak of HPAI (HhN1) was confirmed in Asan, Chungcheongnam-Do, in breeder ducks that had shown a severe drop in egg production but no deaths. During intensive observation within the surveillance zone from the fourth outbreak farm, another HPAI (HhN1) outbreak was confirmed in Cheonan, Chungcheongnam-Do, on January 20, 2007, in a layer chicken farm with a 1% mortality rate (Figure 1). Compared with the rates in the first outbreak, the mortality rates in the more recent outbreaks were low (1%-4%) at notification time. This low proportion of deaths could be attributed to the early reporting system between the farmers and NVRQS, when the mortality rate reached [approximately equal to] 1% of the flock on poultry farms, and to the culling of flocks on reverse transcription–PCR confirmation (usually within 1 day) to prevent the spread of the disease. This could have limited the recorded observations when the infecting influenza virus was eliminated before the full extent of its pathogenicity could be manifested, usually after several days of infection.

Conclusions

Great interest has been focused on the role of migratory birds in the spread of H5N1 subtype and the exchange of virus strains between domestic and wild birds in Asia. Therefore, we surveyed avian influenza virus in migratory birds in South Korea to investigate whether the HPAI (H5N1) outbreaks in domestic poultry bore any relationship to bird migration in the same region. During our routine survey for influenza activity in migratory bird habitats, on December 21, 2006, 2 distinct subtype H5N1 strains were isolated from fecal samples from 2 migratory bird habitats one near the first outbreak farm in Chungcheongnam-Do, and the other from a stream in Chungcheongbuk-Do (Figure 1).

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In Thai provinces where avian influenza outbreaks in poultry had been confirmed in the preceding 6 months, serum from 322 poultry farmers was tested for antibodies to avian influenza virus subtype H5N1 by microneutralization assay. No study participant met the World Health Organization serologic criteria for confirmed infection.

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During late 2003 and 2004, highly pathogenic avian influenza virus (H5N1) caused extensive outbreaks and die-offs in poultry flocks in Thailand and several other countries in Southeast Asia (1). From January through March 2004, 12 cases, 8 fatal, in humans resulted from infection with influenza virus (H5N1) in Thailand (2). In response, the Thailand Department of Livestock Development enlisted government employees to conduct a large-scale cull of poultry in the affected provinces (www.dld. go.th/home/bird_flu/emergency.html). This effort began on January 23, 2004, and resulted in the slaughter of >21 million birds (www.fao.org/ag/againfo/subjects/en/health/ diseases-cards/avian_bg.html). Poultry farmers and persons involved in culling are at increased risk for infection (3). In May 2004, we conducted a seroepidemiologic investigation of Thai poultry farmers to determine the frequency of avian influenza (H5N1) transmission to humans.

The Study

We conducted a cross-sectional study among poultry farmers and cullers from 1 district in each of the 5 provinces (Chachoengsao, Kanchanaburi, Khon Kaen, Sukhothai, and Suphanburi) where outbreaks of avian influenza (H5N1) among poultry and human infections had been confirmed since January 2004 (Figure). With the assistance of provincial human and animal health authorities, we contacted farmers living in these districts. Informed consent was obtained, and a brief interview was conducted. Because the precise timing of potential exposures could not be determined, a single serum sample was collected from each patient and stored at -20[degrees]C until tested under Bio-safety Level 3 (BSL-3) conditions. Specimens were tested, according to adapted methods described by Katz et al. (4), at the Department of Microbiology, Faculty of Medicine, Siriraj Hospital, Mahidol University by Microneutralization assay (micro-Nt) for antibody to H5N1 viruses. Before this study, senior laboratory staff from Siriraj Hospital received 2 weeks of on-site training by a visiting scientist from the US Centers for Disease Control and Prevention who had expertise with this assay. The World Health Organization (WHO) defines a positive test result as a microneutralization antibody titer for influenza virus (H5N1) of >80 with a confirmatory ELISA or Western blot assay (3,4) (www. who.int/csr/disease/avian_influenza/guidelines/case_ definition2006_08_29/en/index.html). Serum samples from persons >50 years of age were excluded from laboratory analysis because the microneutralization assay for antibodies against subtype H5N1 has been reported to be less specific for older persons (5).

[FIGURE OMITTED]

Of 350 farmers asked to participate, 322 (92%) enrolled in the study, of which 167 (52%) were women, and 28 (8%) persons declined to participate. The mean age of participants was 34 years (range 5-50 years) (Table). Among participants, 188 (58%) reported handling sick or dying poultry, 107 (33%) were involved in culling operations of apparently well poultry in outbreak areas, and 27 (9%) reported only contact with well poultry in the context of routine farming practices. Although no study participant had an anti-H5N1 antibody titer of [greater than or equal to] 80, 7 (2.2%) farmers had lower reactive antibody titers. Of these, 4 had titers of 10, 2 had titers of 20, and 1 had a titer of 40. The small number of study participants with anti-H5 antibody titers precluded statistical comparisons to those without reactive antibodies.

Conclusions

Poultry farmers and cullers are at increased occupational risk for exposure to avian influenza viruses. However, since 2004, infections have been less commonly reported in cullers, while poultry farmers have made up a large proportion of cases worldwide. A study in Hong Kong Special Administrative Region, People’s Republic of China, examined influenza virus (H5N1) transmission and risk factors among poultry workers and government workers involved in culling during the 1997-98 outbreak (3). The study concluded that although no hospitalized poultry workers were identified among the 18 patients in that outbreak, 3% of 293 cullers and 10% of 1,525 poultry workers had antibody titers against influenza (H5N1) of [greater than or equal to] 80, which suggested that a substantial number of mild or asymptomatic infections had occurred in this occupationally exposed population. In contrast, we found that no poultry workers had microneutralization titers [greater than or equal to] 80, whereas 7 (2%) had lower titers that did not meet the WHO definition for seropositivity.

These findings could have several possible explanations. The lower titers may have resulted from cross-reactivity with circulating antibodies after previous human influenza virus infections (5,6). These low titers could be the result of mild or asymptomatic influenza (H5N1) infections because not all influenza virus infections invariably result in marked antibody responses (7). Likewise, these results could reflect the decay of antibody titers over time (8). Finally, the Micro-NT assay is a highly specific and strain-sensitive test. Although we used the same virus that was circulating in Thailand at that time, these lower titers could be attributable to infections with another virus variant.

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Perpetuation, overwintering, and extinction of eastern equine encephalitis virus (EEEV) in northern foci are poorly understood. We therefore sought to describe the molecular epidemiology of EEEV in New York State during current and past epizootics. To determine whether EEEV overwinters, is periodically reintroduced, or both, we sequenced the E2 and partial NSP3 coding regions of 42 EEEV isolates from New York State and the Eastern Seaboard of the United States. Our phylogenetic analyses indicated that derived subclades tended to contain southern strains that had been isolated before genetically similar northern strains, suggesting southern to northern migration of EEEV along the Eastern Seaboard. Strong clustering among strains isolated during epizootics in New York from 2003-2005, as well as from 1974-1975, demonstrates that EEEV has overwintered in this focus. This study provides molecular evidence for the introduction of southern EEEV strains to New York, followed by local amplification, perpetuation, and overwintering.

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Eastern equine encephalitis virus (EEEV; genus Alphavirus: family Togaviridae) is maintained in an enzootic cycle between omithophilic mosquitoes and birds. The virus causes disease in some avian hosts and in incidental hosts, such as horses and humans; case-fatality rate in humans is [approximately equal to] 33% (1). Virus activity has been detected in North and South America. In the United States, EEEV has been detected along the Gulf of Mexico and the Atlantic Seaboard as well as in inland foci near the Great Lakes, including upstate New York. The EEEV virion contains a single-stranded, positive-sense RNA genome of [approximately equal to] 12 kb. The 5′ end of the genome encodes 4 nonstructural proteins: NSP1, NSP2, NSP3, and NSP4. The structural proteins are encoded in the 3′ third of the genome and are translated from a subgenomic RNA, 26S, resulting in 5 protein products: C, 6K, E1, E2, and E3 (2). Previous sequencing studies analyzed genetic relationships of EEEV strains in the Western Hemisphere and compared strains distributed across widespread geographic regions (3-6). EEEV has 4 distinct genetic lineages; lineage I consists of highly conserved strains from North America, and lineages II-IV encompass strains from Central and South America (3).

Outbreaks of EEEV in New York have been observed periodically since 1952, when the virus was first detected in pheasants (7). Disease in humans and/or horses has been noted on Long Island, in the lower Hudson Valley, and in central upstate New York; the last known human case in New York occurred in 1983 in Onondaga County (8). Most EEEV activity in New York has occurred in counties bordering Oneida Lake in central upstate New York (Figure 1). Most of the activity in this region has been concentrated in the Big Bay-Toad Harbor Swamp complex in Oswego County and Cicero Swamp in Onondaga County (8). Culiseta melanura (Coquillett), the main enzootic vector of EEEV, breeds abundantly in these swamps (9). Localized epizootics in the counties of Oswego and Onondaga have been documented in a transmission focus during 1971-1977, 1982-1983, and 1990-1991 (8,10-13) and from 2003 to the present (2007; D.S. Young et al., unpub, data). Between these epizootic periods, EEEV was undetectable in horses and birds and only infrequently detected in mosquito pools (D.S. Young et al., unpub, data) (8). From 1992 through 1997 in upstate New York, EEEV was detected in 18 mosquito pools from Onondaga County (1994) and 3 mosquito pools from Oswego County (1996); no equine or avian cases were detected (D.S. Young et al., unpub. data). From 1998 through 2002, EEEV was not detected in mosquitoes or vertebrates in New York. However, in 2003, EEEV activity increased across New York with the emergence of the current epizootic (2003-2007) in the Onondaga and Oswego Counties region.

[FIGURE 1 OMITTED]

Patterns of localized perpetuation, overwintering, and extinction of EEEV in transmission foci are poorly understood. To determine whether EEEV overwinters locally in temperate regions such as upstate New York or whether annual reintroduction is required to reinitiate the transmission cycle, we compared nucleotide sequences comprising the entire E2 coding region and part of the NSP3 coding region. We examined 35 strains isolated in New York during 1971-1975 and 2003-2005 and 7 strains collected along the Eastern Seaboard of the United States during 2002-2003. Using these data, we described the molecular epidemiology of EEEV strains collected during the current and past epizootics in New York.

Materials and Methods

EEEV Detection and Isolation

Isolates from New York State and the Eastern Seaboard were sequenced for this study (online Appendix Table, available from www.cdc.gov/EID/content/14/3/454-appT.htm). Strains originating outside of New York were isolated from avian serum samples, which were collected during a study conducted by the US Geological Survey and stored at -80[degrees]C until inoculation onto cell culture. All EEEV strains from within New York were collected from mosquito, avian, and equine samples that were submitted to the Wadsworth Center’s Arbovirus Laboratories as a part of surveillance efforts by the New York State Department of Health. EEEV strains isolated during 1971-1975 were obtained from our archives.

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In the absence of a fully effective Herpes simplex virus (HSV) vaccine, topical microbicides represent an important strategy for preventing HSV transmission. (-) Epigallocatechin gallate (EGCG) (MW 458.4) is the primary catechin in green tea. The present study shows that EGCG has greater anti-HSV activity than other green tea catechins and inactivates multiple clinical isolates of HSV-1 and HSV-2. EGCG reduced HSV-2 titers by >/= 1,000-fold in 10-20 minutes and reduced HSV-1 titers by the same amount in 30-40 minutes. The anti-HSV activity of EGCG is due to a direct effect on the virion, and incubating Vero and CV1 cells with EGCG for 48 hours prior to infection with HSV-1 and HSV-2 respectively does not reduce HSV production. Electron microscopical (EM) studies showed that purified virions exposed to EGCG were damaged and EM immunogold labelling of the envelope glycoproteins gB and gD was significantly reduced following EGCG treatment while capsid protein labelling was unchanged. When the purified HSV-1 envelope glycoproteins gB and gD were incubated with EGCG and then examined by SDS gel electrophoresis, lower molecular weight gB and gD bands decreased and new higher molecular weight bands appeared indicating the EGCG dependent production of macromolecular complexes, gB and gD are essential for HSV infectivity and these results suggest that EGCG could inactivate HSV virions by binding to gB, gD or another envelope glycoprotein. EGCG is stable in the pH range found vaginally and appears to be a promising candidate for use in a microbicide to reduce HSV transmission.

Antimicrob Agents Chemother 2008 Jan 14; [Epub ahead of print]

COPYRIGHT 2008 Thorne Research Inc.
COPYRIGHT 2008 Gale, Cengage Learning

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Segmented double-stranded RNA viruses; structure and molecular biology.

Ed. by John T. Patton.

Caister Academic Press

2008

394 pages

$300.00

Hardcover

QR395

Recent advances in determining the atomic and subnanometer capsid structures of double-stranded (ds) RNA viruses and the structures of a number of individual viral proteins have provided insight into events in the viral life cycle, including attachment and entry, genome replication, gene expression, and capsid morphogenesis. Patton (Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases) presents 20 articles reviewing current knowledge in this area, primarily from the perspective of the structure and related functions of capsids and individual viral protein products. Specific topics include the structure of orthoreoviruses, cypovirus, rotavirus structure, structure and function of bluetongue virus and its proteins, structures of phytoreoviruses, dissecting the assembly pathway of bacterial dsRNA viruses, infectious bursal disease virus, structural basis of mammalian orthoreovirus cell attachment, rotavirus cell entry, entry of a segmented dsRNA virus into the bacterial cell, analyses of rotavirus NSP4 genetic groups and structure, and genomic RNA packaging and replication in the Cystoviridae. Distributed in the US by ISBS.

([c]20082005 Book News, Inc., Portland, OR)

COPYRIGHT 2008 Book News, Inc.
COPYRIGHT 2008 Gale, Cengage Learning

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Parainfluenza virus (PIV) is a leading cause of respiratory infections in humans. A novel virus closely related to human and bovine parainfluenza viruses types 3 (HPIV-3 and BPIV-3), named Tursiops truncatus parainfluenza virus type 1 (TtPIV-1), was isolated from a dolphin with respiratory disease. We developed a dolphin-specific ELISA to measure acute- and convalescent-phase PIV antibodies in dolphins during 1999-2006 with hemograms similar to that of the positive control. PIV seroconversion occurred concurrently with an abnormal hemogram in 22 animals, of which 7 (31.8%) had respiratory signs. Seroprevalence surveys were conducted on 114 healthy bottlenose dolphins in Florida and California. When the most conservative interpretation of positive was used, 11.4% of healthy dolphins were antibody positive, 29.8% were negative, and 58.8% were inconclusive. PIV appears to be a common marine mammal virus that may be of human health interest because of the similarity of TtPIV-1 to BPIV-3 and HPIV-3.

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Parainfluenza viruses (PIVs) are often associated with respiratory illness in terrestrial mammals, including croup in humans (1), kennel cough in dogs (2), and bovine respiratory disease in cattle (3). A novel PIV tentatively named Tursiops truncatus parainfluenza virus type 1 (TtPIV-1) was cultured from lung tissue in an Atlantic bottlenose dolphin (T. truncatus) (4). This animal had respiratory disease including laryngitis, tracheitis, and bronchointerstitial pneumonia with mild to moderate growth of Candida glabrata.

Phylogenetic analyses of 2 genomic fragments of TtPIV-1 showed that the virus strain was monophyletic with, but genetically distinct from, bovine parainfluenza virus 3 (BPIV-3) strains and human parainfluenza type 3 (HPIV-3) (4). BPIV-3 is an effective antigenic stimulator in humans and is used in human vaccines that protect against HPIV-3 (5 7). TtPIV-1 may provide similar protection in humans. Dolphins have been recognized as useful marine ecosystem sentinels (8), and changes in marine PIV may reflect changes in terrestrial PIV.

ELISAs have been characterized as the most sensitive diagnostic tool to identify rising titers due to PIV-associated respiratory illness in humans (9). Although ELISA is the ideal tool for identifying infections caused by PIV, high levels of antigenic cross-reactivity among various PIV subfamilies and other closely related viruses hinder the ability for ELISA to determine which type of PIV has infected an animal (10,11). In wild marine mammal populations, ELISA-based serosurveys for suspected viral or bacterial pathogens are common (12-14). Limitations of these studies include unknown health status of animals or lack of paired samples that can differentiate exposures from active infections.

The US Navy Marine Mammal Program (MMP) manages a population of bottlenose dolphins that live in San Diego Bay, California. These animals are provided high-quality medical and preventive care throughout their lifetime. Standardized health data and voluntary blood samples are collected routinely, uniquely enabling MMP to amass routine physiologic information on dolphins living in a marine environment at all age stages. Since 1988, health assessments have been conducted by the Chicago Zoological Society and collaborators on a free-ranging, resident coastal population of bottlenose dolphins in Sarasota Bay, Florida, 2,500 miles away, as part of the world’s longest running study of wild dolphins. Serum samples from this presumably healthy population are archived for use in retrospective health assessments.

An indirect, dolphin-specific PIV-antibody ELISA was developed and applied to archived serum samples collected from MMP dolphins in San Diego (1999-2006) and healthy, flee-ranging dolphins living near Sarasota (20042005). We used this ELISA to assess the clinical relevance of PIV exposure and seroconversion in bottlenose dolphins living along US coasts.

Methods

The MMP is routinely reviewed by an Institutional Animal Care and Use Committee (IACUC) and Navy Bureau of Medicine; the MMP is accredited by the Assessment and Accreditation of Laboratory Care International. All sample collection protocols for the Sarasota wild dolphin population were approved by the University of Florida IACUC (IACUC no. C233).

San Diego, California

Blood samples from MMP dolphins were initially collected by venipuncture from animals trained either to present their tail for sampling in the water or to rest on a foam mat during a routine physical examination out of the water. Samples were collected from the caudal peduncle vein by using a 20- or 21-gauge, 1.5-inch Vacutainer needle (Becton Dickinson Vacutainer Systems, Rutherford, N J, USA) or from a fluke vein by using a 21-gauge, 1-inch butterfly needle. Blood was collected into a Vacutainer serum separator tube or a Vacutainer EDTA ([K.sub.3]) tube for serum chemistries and complete blood counts, respectively.

Samples for chemistry analysis were centrifuged within 2 h of collection. Centrifugation was performed at 3,000 rpm at 21[degrees]C for 10 min. Fibrin clots were removed, and serum was transferred to a 5-mL plastic submission tube. Whole blood was collected in EDTA Vacutainer tubes. All samples were sent on wet ice by courier to Quest Diagnostic Laboratories in San Diego.

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We report mutations in influenza A virus (H5N1) strains associated with 2 outbreaks in Turkey. Four novel amino acid changes (Q447L, N556K, and R46K in RNA polymerase and S133A in hemagglutinin) were detected in virus isolates from 2 siblings who died.

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Influenza A virus (H5N1) is the predominant candidate for a future influenza pandemic if it develops efficient ability for human-to-human transmission. Since 2003, a total of 109 human deaths have been associated with this strain (1). Monitoring the genetic structure of this virus is needed for predicting changes that may confer ability to cause pandemics: pathogenicity, host range, and antigenic drift.

Recently, 2 avian influenza A (H5N1) outbreaks occurred in Turkey. The first outbreak, in Balikesir in northwestern Turkey in October 2005, was limited to poultry. The second outbreak, in Dogubeyazit in northeastern Turkey in November 2005, involved poultry and humans. As of January 2006, a total of 12 human cases, 4 fatal, have been confirmed (1).

The Study

We analyzed molecular evolution of the virus genome by sequencing the hemagglutinin (HA