“Severe lung infection was a hallmark of the illness produced by the original pandemic virus in humans, suggesting a possible, though not conclusive, association between the pandemic virus HA and its pathogenicity in humans, and indicating the need to examine the contribution of the HA to viral pathogenicity in other animal models,” the report says. An international team of researchers recreated hemagglutinin (HA) from the 1918 “Spanish flu” virus and spliced it into recent flu viruses adapted to humans and mice, according to a recent report in Nature. Mice that were exposed to the engineered viruses suffered severe lung infections that resembled those seen in people who died in the 1918 pandemic, according to the report. “Replacing only one gene is sufficient to make the virus more pathogenic,” said senior author Yoshihiro Kawaoka, a virologist at the University of WisconsinMadison (UWM) and the University of Tokyo, in a news release from UWM. Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, recently concurred that there is more to be learned about what made the 1918 virus so destructive. “It is very clear that there was something about the virulence of this microbe that we don’t fully understand,” he said in a Nov 15 press briefing on flu research. To do this, they took three recent influenza A strains (one of which is pathogenic in mice and two of which are not) and replaced their HA and NA genes either with the 1918 versions of both genes or with the 1918 HA gene and an NA gene from a recent strain. They then exposed groups of mice to the engineered viruses or the three natural viruses by intranasal inoculation. In postmortem examinations, the researchers found signs that infection had spread much deeper into the lungs in mice exposed to viruses containing the 1918 HA gene than in the other mice. The researchers also report evidence that people who were alive in 1918 still have immunity to the 1918 virus. They examined the neutralizing activity of blood serum samples from people of various ages against viruses with the 1918 HA and NA genes and against more recent human flu viruses. Serum from those who survived the pandemic “showed markedly high activities” against the engineered virus, while samples from younger people had only limited activity against it. Despite their findings, Kawaoka and colleagues say that HA is probably not the sole cause of the virulence of the 1918 virus. “The virulence of influenza virus is probably a polygenic trait, in that ultimately we expect other gene products . . . to be implicated in the phenotype of the 1918 virus,” they write. “These highly virulent recombinant viruses expressing the 1918 viral HA could infect the entire lung and induce high levels of macrophage-derived chemokines and cytokines, which resulted in infiltration of inflammatory cells and severe haemorrhage, hallmarks of the illness produced during the original pandemic,” the abstract of the report states. Further, the addition of the 1918 HA gene to a virus that is normally pathogenic in mice made the lung lesions “clearly more severe” than those in mice infected with the normal version of the virus. What made the 1918 virus so lethal has been a mystery. The report by Kawaoka and colleagues says speculation has focused on living conditions at the end of World War I as well as on properties of the virus itself. The HA and NA of the virus contain no amino acid sequences known to be linked with high virulence, the report says. The researchers therefore sought to test the effects of the 1918 virus HA and NA on the pathogenicity of flu viruses in mice. Nov 24, 2004 (CIDRAP News) By recreating a key surface protein from the 1918 pandemic flu virus and testing its effects in mice, researchers have shown that the protein might have been an important reason for the virus’s extraordinary ability to kill. All the viruses containing the 1918 HA gene, including those that in their natural form are harmless to mice, grew quickly in the mice’s lungs and eventually killed them, according to the report. Viruses containing both HA and NA from the 1918 virus were no more harmful than those containing the 1918 HA along with NA from a recent strain, which indicated that the 1918 version of NA didn’t contribute to viral pathogenicity. The 1918 flu pandemic killed tens of millions of people around the world. In recent years, researchers have extracted several of the virus’s genes from preserved tissue samples from pandemic victims and have sequenced them. HA and neuraminidase (NA), surface proteins that equip flu viruses to enter and leave human cells, are important targets of the body’s immune response; changes in their structure can make the virus more dangerous and enable it to infect new species. Kawaoka’s group also looked at the ability of 1918 viral HA to recognize the cell-surface receptor molecule preferred by human-adapted flu viruses. Using a “competitive binding assay,” the team found that the 1918 HA preferentially recognizes this receptor. Because the 1918 virus is believed to have originated in birds, this finding suggests that the virus must have circulated in humans long enough to develop a preference for the human type of receptor, the article says. Kobasa D, Takada A, Shinya K, et al. Enhanced virulence of influenza A viruses with the haemagglutinin of the 1918 pandemic virus. Nature 2004;431:703-7 [Abstract] If the 1918 virus reemerged today, “The only group with significant natural protection would be survivors of the 1918 pandemic, who still express high levels of antibodies against an antigen to which they were exposed over 80 years ago, a phenomenon referred to as original antigenic sin,” the report says.
HashChing has found homeowners in seven Queensland suburbs were paying as high as 7.39 per cent in interest on their mortgages.SEVEN Queensland suburbs were named in a line-up of places where homeowners pay too much in interest rates – but it was a Brisbane suburb that won the refinance battle. Latest data from online platform HashChing found homeowners in Brendale, Coomera, Advancetown, Austinville, Labrador, Surfers Paradise and Springbrook were paying off mortgages with rates as high as 7.39 per cent.That was 2.67 percentage points higher than the Brisbane average (4.72 per cent), but they weren’t the only ones footing a higher bill than necessary.More from newsMould, age, not enough to stop 17 bidders fighting for this home3 hours agoBuyers ‘crazy’ not to take govt freebies, says 28-yr-old investor9 hours agoHashChing found that self employed borrowers were paying higher interest rates (5.71 per cent) on average – that was almost a whole percentage point higher than PAYG borrowers.But some parts of Brisbane have been making strong moves to lock in record low interest rates, with Everton Park emerging as the most refinanced postcode in Queensland. Everton Hills and Mitchelton share the same postcode (4053)., with the area averaging a loan amount of $482,334 at an interest rate of 4.89 per cent.Other Brisbane suburbs that saw the state’s strongest refinancing applications were Cashmere, Joyner, Bray Park, Warner, Brendale (4500 postcode), Carole Park, Goodna, Bellbird Park, Brookwater, Springfield Lakes (4300 postcode), Murrumba Downs, Griffin, Dakabin and Kallangur (4503).On the Gold Coast, there was a big push towards refinancing out of Arundel, Parkwood, Molendinar (4214 postcode), Broadbeach Waters, Broadbeach, Mermaid Waters, Mermaid Beach (4218 postcode), Pacific Pine, Nerang (4211 postcode), Labrador, Southport (4215 postcode).HashChing found the average refinance amount in the state was $497,881.Westpac was the only major bank whose refinancing average ($521,102) came in higher than the state average, though CBA was receiving the most applications (23.3 per cent), with ANZ and Westpac on a fifth each and NAB seeing 15.8 per cent..
ORVC Weekly Report (December 10 – 15)Players of the Week.Girls Basketball: Elexah Roepke – South Ripley and Abby Ralston – SouthwesternBoys Basketball: Foster Mefford – SouthwesternORVC Report(December 10-15)2018Courtesy of ORVC Recorder Travis Calvert.
Ghana has not been seeded ahead of Friday’s draw for the 2019 Africa Cup of Nations.The Black Stars, instead, have dropped to Pot 2, complicating the country’s path to a first AFCON success since 1982.Host nation Egypt, defending champions Cameroon, have been seeded while Senegal, Tunisia, Nigeria and Morocco join the list of six (6) seeded countries for the 24-team tournament.The draw procedure was approved at the CAF Executive Committee Meeting on Thursday in Cairo, having been proposed by the Organising Committee of the Total Africa Cup of Nations.The selection of the seeded teams was based on the latest FIFA ranking of the teams. Despite being ranked the 6th best team on the continent, both Cameroon and Egypt, being ranked outside the top 6 in Africa means they take the place of the Black Stars and DR Congo, pushing them into Pot 2.Ghana will be joined in Pot 2 by DR Congo, Mali, Cote d’Ivoire, Guinea and Algeria.Full AFCON 2019 Draw Pots:Pot 1: Egypt, Cameroon, Senegal, Tunisia, Nigeria, MoroccoPot 2: DR Congon, Ghana, Mali, Cote d’Ivoire, Guinea, AlgeriaPot 3: South Africa, Uganda, Benin, Mauritania, Madagascar, KenyaPot 4: Zimbabwe, Namibia, Guinea Bissau, Angola, Tanzania, BurundiDraw Procedure:According to the Article 73.1 of the regulations of the competition;– The organizing country (Egypt) shall be the head of group A.– The holder of the trophy (Cameroon) will be the head of one of the five other groups inaddition to 4 other head of groups determined in accordance to the ranking.Procedures of the draw:The following 4 pots will be on stage:Pot 4: Containing the 6 teams of level IVPot 3: Containing the 6 teams of level IIIPot 2: Containing the 6 teams of level IIPot 1: Containing the 5 teams of level I (Host country is in position A1)Step 1:Pot 4: The 6 less seeded teams of level IV will be in pot 4o The first ball drawn will go directly to group A; in position A4.o The second ball drawn will go directly to group B; in position B4o The third ball drawn will go directly to group C; in position C4o The fourth ball drawn will go directly to group D; in position D4o The fifth ball drawn will go directly to group E; in position E4o The sixth ball drawn will go directly to group F; in position F4Step 2:Pot 3: The 6 teams of level III will be in pot 3o The first ball drawn will go directly to group A; in position A3.o The second ball drawn will go directly to group B; in position B3o The third ball drawn will go directly to group C; in position C3o The fourth ball drawn will go directly to group D; in position D3o The fifth ball drawn will go directly to group E; in position E3o The sixth ball drawn will go directly to group F; in position F3
A month-by-month look at the Angels’ 2018 scheduleMARCH29 at Oakland, 1 p.m.30 at Oakland, 7 p.m.31 at Oakland, 1 p.m.APRIL1 at Oakland, 1 p.m.2 Cleveland, 7 p.m.3 Cleveland, 7 p.m.4 Cleveland, 1 p.m.6 Oakland, 7 p.m.7 Oakland, 6 p.m.8 Oakland, 1 p.m.9 at Texas, 5 p.m.10 at Texas, 5 p.m.11 at Texas, 5 p.m.12, at Kansas City, 5:15 p.m.13 at Kansas City, 5:15 p.m.14 at Kansas City, 4:15 p.m.15 at Kansas City, 11:15 a.m.17 Boston, 7 p.m.18 Boston, 7 p.m.19 Boston, 7 p.m.20 San Francisco, 7 p.m.21 San Francisco, 6 p.m.22 San Francisco, 1 p.m.23 at Houston , 5 p.m.24 at Houston, 5 p.m.25 at Houston, 11 a.m.27 NY Yankees, 7 p.m.28 NY Yankees, 6 p.m.29 NY Yankees, 5 p.m.MAY1 Baltimore, 7 p.m.2 Baltimore, 7 p.m.3 Baltimore, 7 p.m.4 at Seattle, 7 p.m.5 at Seattle, 6 p.m.6 at Seattle, 1 p.m.8 at Colorado, 5:30 p.m.9 at Colorado, noon10 Minnesota, 7 p.m.11 Minnesota, 7 p.m.12 Minnesota, 6 p.m.13 Minnesota, 1 p.m.14 Houston, 7 p.m.15 Houston, 7 p.m.16 Houston, 6:30 p.m.17 Tampa Bay, 7 p.m.18 Tampa Bay, 7 p.m.19 Tampa Bay, 6 p.m.20 Tampa Bay, 1 p.m.22 at Toronto, 4 p.m.23 at Toronto, 4 p.m.24 at Toronto, 9:30 a.m.25 at NY Yankees, 4 p.m.26 at NY Yankees, 4:15 p.m.27 at NY Yankees, 10 a.m.28 at Detroit, 10 a.m.29 at Detroit, 4 p.m.30 at Detroit, 4 p.m.31 at Detroit, 10 a.m. JUNE1 Texas, 7 p.m.2 Texas, 6 p.m.3 Texas, 1 p.m.4 Kansas City, 7 p.m.5 Kansas City, 7 p.m.6 Kansas City, 7 p.m.8 at Minnesota, 5 p.m.9 at Minnesota, 11 a.m.10 at Minnesota, 11 a.m.11 at Seattle, 7 p.m.12 at Seattle, 7 p.m.13 at Seattle, 1 p.m.15 at Oakland, 6:30 p.m.16 at Oakland, 1 p.m.17 at Oakland, 1 p.m.18 Arizona, 7 p.m.19 Arizona, 7 p.m.21 Toronto, 7 p.m.22 Toronto, 7 p.m.23 Toronto, 6 p.m.24 Toronto, 1 p.m.26 at Boston, 4 p.m.27 at Boston, 4 p.m.28 at Boston, 4 p.m.29 at Baltimore, 4 p.m.30 at Baltimore, 1 p.m.JULY1 at Baltimore, 10 a.m.3 at Seattle, 7 p.m.4 at Seattle, 1 p.m.5 at Seattle, 7 p.m.6 Dodgers, 7 p.m.7 Dodgers, 4:15 p.m.8 Dodgers, TBD10 Seattle, 7 p.m.11 Seattle, 7 p.m.12 Seattle, 7 p.m.13 at Dodgers, 7 p.m.14 at Dodgers, 4:15 p.m.15 at Dodgers, 1 p.m.20 Houston, 7 p.m.21 Houston, 4:15 p.m.22 Houston, 1 p.m.23 White Sox, 7 p.m.24 White Sox, 7 p.m.25 White Sox, 7 p.m.26 White Sox, 1 p.m.27 Seattle, 7 p.m.28 Seattle, 6 p.m.29 Seattle, 1 p.m.31 at Tampa Bay, 4 p.m.AUGUST1 at Tampa Bay, 4 p.m.2 at Tampa Bay, 10 a.m.3 at Cleveland, 4 p.m.4 at Cleveland, 4 p.m.5 at Cleveland, 10 a.m.6 Detroit, 7 p.m.7 Detroit, 7 p.m.8 Detroit, 1 p.m.10 Oakland, 7 p.m.11 Oakland, 6 p.m.12 Oakland, 1 p.m.13 at San Diego, 7 p.m.14 at San Diego, 7 p.m.15 at San Diego, 6 p.m.16 at Texas, 5 p.m.17 at Texas, 5 p.m.18 at Texas, 5 p.m.19 at Texas, noon21 at Arizona, 6:30 p.m.22 at Arizona, 6:30 p.m.24 Houston, 7 p.m.25 Houston, 6 p.m.26 Houston, TBD27 Colorado, 7 p.m.28 Colorado, 7 p.m.30 at Houston, 5 p.m.31 at Houston, 5 p.m.SEPTEMBER1 at Houston, 4 p.m.2 at Houston, 11 a.m.3 at Texas, 5 p.m.4 at Texas, 5 p.m.5 at Texas, 5 p.m.7 at White Sox, 5 p.m.8 at White Sox, 4 p.m.9 at White Sox, 11 a.m.10 Texas, 7 p.m.11 Texas, 7 p.m.12 Texas, 7 p.m.13 Seattle, 7 p.m.14 Seattle, 7 p.m.15 Seattle, 6 p.m.16 Seattle, 1 p.m.18 at Oakland, 7 p.m.19 at Oakland, 7 p.m.20 at Oakland, 12:30 p.m.21 at Houston, 5 p.m.22 at Houston, 4 p.m.23 at Houston, 11 a.m.24 Texas, 7 p.m.25 Texas, 7 p.m.26 Texas, 7 p.m.28 Oakland, 7 p.m.29 Oakland, 6 p.m.30 Oakland, noon Newsroom GuidelinesNews TipsContact UsReport an Error