Via Scoop.it – Virology News
Meta-analyses of the few studies providing effects with adjustment for confounders suggest that in high-risk populations, oral oseltamivir may reduce mortality (odds ratio, 0.23 [95% CI, 0.13 to 0.43]; low-quality evidence), hospitalization (odds ratio, 0.75 [CI, 0.66 to 0.89]; low-quality evidence), and duration of symptoms (33 hours [CI, 21 to 45 hours]; very low–quality evidence) compared with no treatment. Earlier treatment with oseltamivir was generally associated with better outcomes. Inhaled zanamivir may lead to shorter symptom duration (23 hours [CI, 17 to 28 hours]; moderate-quality evidence) and fewer hospitalizations (odds ratio, 0.66 [CI, 0.37 to 1.18]) but more complications than no treatment. Direct comparison of oral oseltamivir and inhaled zanamivir suggests no important differences in key outcomes. Data from 1 study suggests that oral amantadine may reduce mortality and pneumonia associated with influenza A. No included study evaluated rimantadine. Image courtesy of Russell Kightley Media
Via www.annals.org
Archive for February, 2012
Antivirals for Treatment of Influenza: A Systematic Review and Meta-analysis of Observational Studies
28 February, 2012allAfrica.com: South Africa: New Reports Chart Progress – and Costs – in HIV Fight
28 February, 2012Via Scoop.it – Virology News
Although in its sixth year of publication, this year’s barometer is the first to include data on early infant HIV testing for babies born to HIV-positive mothers and shows that about half of all babies born to HIV-positive mothers are now being tested for the virus at six weeks of age, an important step to ensuring they access the early HIV treatment recommended for all children younger than one under national guidelines. In 2009, only about a quarter of such babies were being tested using the sensitive polymerase chain reaction – tests that confirm whether HIV-exposed infants are HIV-positive. The report also found that almost all pregnant women are now tested for HIV, which has helped lower mother-to-child HIV transmission to below 4 percent in the country.
Via allafrica.com
Mmegi Online :: Facebook is the new front in HIV/AIDS war
28 February, 2012Via Scoop.it – Virology News
FRANCISTOWN: Poor knowledge about HIV/Aids and other sexually transmitted diseases among young people has compelled a Gaborone-based youth to create a group on the popular social network, Facebook, to enlighten his peers about the scourge. Ex Africa, semper aliquid novi. Or a Facebook page, in this case.
Via www.mmegi.bw
Flu Virus Discovered In Bats
28 February, 2012Via Scoop.it – Virology News
Scientists from the US Centers for Disease Control and Prevention (CDC) have discovered evidence of a new influenza type A virus in Guatemalan fruit bats. “…for reassortment to occur, the bat flu virus would have to be capable of infecting a different animal, such as a pig, horse or dog, at the same time as a human flu virus. So far, the bat flu virus has only been found in little yellow-shouldered bats. These fruit bats are not native to the US, but quite common in Central and South America. The bats don’t bite people, but it is feasible they could shed the virus onto foods like fruit and vegetables that are then eaten by humans and other animals.” And if you watched “Contagion”, you will rmember the bulldozer knocking down the tree, which disturbed the bat, which roosted in a pigpen, where pigs ate the faeces, and – recombination occurred!
Via www.medicalnewstoday.com
HIV epidemic “driven by colonialism in Africa” a century ago
28 February, 2012Via Scoop.it – Virology News
Tinderbox: How the West Sparked the AIDS Epidemic and How the World Can Finally Overcome It, attempts to pinpoint the birth and early life of HIV and AIDS. Considering a wealth of evidence, the authors suggest that the European Scramble for Africa during the late 19th and early 20th century helped turn localised outbreaks of the infection into a global epidemic.
Read more: http://www.dailymail.co.uk/health/article-2107605/HIV-epidemic-driven-colonialism-Africa-century-ago.html#ixzz1nhlAqwEM
Via www.dailymail.co.uk
Weaponising bird flu? We don’t need to weaponise no bird flu….
28 February, 2012Via Scoop.it – Virology News
My family and I just watched “Contagion” on pay TV – and were most impressed. Reasonably true to life, all sorts of realistic scenarios, Ian Lipkin appearing as an extra – and one wonderful quote: “Someone doesn’t have to weaponise the bird flu. The birds are doing that”. Contagion is only a movie – but that’s so true. Oh, and an uncredited appearance by Darren Martin’s wonderful recombination analysis package, RDP 2.0 – at 1hr 15 min from the end.
The origin of HIV: still so much garbage out there
20 February, 2012While curating Virology News today, I came across another reprocessing of new that I had come across earlier concerning apparent natural protection of some African female sex workers against HIV infection: this was the intriguingly-entitled “African women’s genitals provide clue to HIV prevention“, in what appears to be an online Nigerian newspaper.
This recapitulates, very accurately, the information I reported in Virology News, which was the subject of a news release following the publication in the September 2011 edition of PLoS One of a study entitled “High Level of Soluble HLA-G in the Female Genital Tract of Beninese Commercial Sex Workers Is Associated with HIV-1 Infection”. The gist of this is that:
“HIV-resistant sex workers in Africa have a weak inflammatory response in their vaginas – a surprise for the researchers, who were expecting the contrary considering the women’s high exposure to the virus.”
This may lend further credence to the observation that progression to AIDS in HIV-infected people is associated with a state of chronic immune activation – and that SIV-infected vervet monkeys do not exhibit such chromic immune activation, and do not progress like humans do.
What is interesting about the Nigerian article, however, is not what it reports – it is the online comments that follow it. Here is a selection:
“Was HIV realy discovered in Africa ? Forget the western media propaganda . I have believed , for years , that HIV is a laboratory virus designed for genocide in the thick of apartheid inhuman policies in South Africa .”
“Neither did HIV originate nor was it perculiar to Africa. It was the creation of the Western countries to stsyematically reduce African population. that the subjects of this study were exposed to HIV virus attests to this fact.”
And my personal favourite:
“So you have already swallowed up the white propaganda that the AIDS virus was first discovered in 1981 in a remote area of central Africa in the green monkey! A fairy tale, which never explains why prior to its first clinical detection among western homosexual men in the late seventies, no case was found in Africans, and no animal or human population died off in Africa, yet the homosexual population of the west was seriously threatened until their protected sex campaign took off.
You must be unaware that about 35 years ago the Soviet KGB told the world the truth about AIDS….
Jakob Segal, a former biology professor at Humboldt University in then-East Germany, proposed that HIV was engineered at a U.S. military laboratory at Fort Detrick, by splicing together two other viruses, Visna and HTLV-1. According to his theory, the new virus, created between 1977 and 1978, was tested on prison inmates who had volunteered for the experiment in exchange for early release. He further suggested that it was through these prisoners, most of who were homosexuals, that the virus was spread to the population at large.”
What is depressing is that there is just one comment saying “…where HIV started is of little significance now. the issue is that our brothers Africans are the ones affected so we must work hard to find the cure and save our brothers.”
What is obvious is that, even in an environment such as one of the most developed nations in Africa, where intelligent science reporting is happening, the public seems to be alarmingly misinformed about the origin of HIV and predisposed to believe racist conspiracy theories that were debunked years ago.
FACT:
HIV did not come from “green monkeys” and was not discovered in 1981: the virus was described in 1983 and 1984, and HIV entered the human population in central Africa multiple times, from chimpanzees and possibly also from gorillas, almost certainly via bushmeat – and this happened in the 1930s or even earlier.
FACT:
HIV could not possibly have resulted from the splicing together of Visna virus and HTLV-1, as no HIV sequence bears any strong resemblance to either virus – and especially not to both of them in different parts of their genomes, as they would be expected to if they were artificial recombinants. Moreover, the first HIV that has been reliably dated comes from a sample taken in the Congo in 1959.
All of these facts can be easily discovered by a trawl of either the scientific literature, or a first-level digest of that literature by reputable journalists. All else is fiction…and malicious fiction at that, whether or not such supposed luminaries as Thabo Mbeki believe it.
12th May 2015
ANOTHER note added in response to Timothy Julian, below, who seems not to understand anything about retrovirus and especially lentivirus evolution. Here is an unrooted radial relationship diagram (aka “phylogenetic” diagram) depicting whole genome sequence relationships between HIV-1, HIV-2, 2 SIVs, Maedi-Visna ad bovine leukaemia viruses, feline and bovine immunodeficiency and human and simian T-cell lymphotropic viruses. Done by me today from Genbank sequences, using CLC Genomics Workbench ver 7.
What it shows is that:
- there is a distinctive clustering of HIVs and of SIVs, with MVV as a apparently closer relative than the FIVs, in a cluster of lentiviruses that includes BIV – and I note HIV-1 is more closely related to an SIV than it is to HIV-2, and there are three branches to the H/SIV tree ALL of which are internal to MVV and the FIVs and BIV.
- the H/STLVs cluster together as relatives, with HTLV-1/2/3 being most closelt related to STLV-1/2/3 – which, seeing as the HTLVs are supposed to have derived from the STLVs, is hardly surprising.
- BLV is only distantly related to the TLV cluster, as is expected given that it is a leukaemia virus but one of a very different species
If HIV-1 derives from artificial constructs derived from FIVs, which are less closely related to them than is MVV, then is the same true for the whole primate cluster? Really? When it is pretty obvious that they are (a) evolutionarily related most closely to one another, (b) evolutionarily diverged to quite a considerable extent? So were they all made individually?? Then cleverly given to different bush-dwelling primates in Africa? How desperately unlikely is that?? You appear not to have heard of teh principle of parsimony, which is that the simplest explanation that covers all of the facts is probably correct – which in this case, is that both HIVs and all of the SIVs have a common evolutionary origin, thousands of years ago – and that all lentiviruses also have a common origin, millions of years ago.
Seriously, Timothy: give it a rest. You know less than Jon Snow.
A life in Virology
15 February, 2012With a group of my UCT Medical School colleagues, I have been attending reasonably regular informal talks by Professor Keith Dumbell, formerly of St Mary’s Hospital, London, the University of Liverpool, and UCT.
Keith is a poxvirus expert, and was involved in the eradication of smallpox. He has also lived through several eras of modern virology, starting in 1945 in the pre-DNA and electron microscope days, through the advent of tissue culturing viruses, to the application of recombinant DNA techniques to viruses – and has a treasure trove of fascinating stories he is sharing with us.
Mostly about viruses, but occasionally about the characters involved as well. And the fact that any virologist worth their salt in the 1950s had to have skills in cutting sections, culturing viruses in eggs, centrifugation techniques, and keeping a veritable zoo of small animals.
I hope to get his permission to release a DVD of his reminiscences some day.
Scoop.it: Virology News
11 February, 2012This is just to announce that I will be regularly posting “Virology News” updates on a new Scoop.it site I have just set up – as well as occasionally updating another Scoop.it site – “Virology and Bioinformatics from Virology.ca” – which is curated by Chris Upton, of Univ Victoria in Canada.
Even more ways to get your daily viral fix…B-)
And while they were arguing about killer H5N1…
8 February, 2012…Elsevier’s Virology was calmly publishing another paper on a “mutant” H5N1….
The abstract:
Acquisition of α2-6 sialoside receptor specificity by α2-3 specific highly-pathogenic avian influenza viruses (H5N1) is thought to be a prerequisite for efficient transmission in humans. By in vitro selection for binding α2-6 sialosides, we identified four variant viruses with amino acid substitutions in the hemagglutinin (S227N, D187G, E190G, and Q196R) that revealed modestly increased α2-6 and minimally decreased α2-3 binding by glycan array analysis. However, a mutant virus combining Q196R with mutations from previous pandemic viruses (Q226L and G228S) revealed predominantly α2-6 binding. Unlike the wild type H5N1, this mutant virus was transmitted by direct contact in the ferret model although not by airborne respiratory droplets. However, a reassortant virus with the mutant hemagglutinin, a human N2 neuraminidase and internal genes from an H5N1 virus was partially transmitted via respiratory droplets. The complex changes required for airborne transmissibility in ferrets suggest that extensive evolution is needed for H5N1 transmissibility in humans. [my emphasis – Ed]
I have covered the use of glycan arrays to characterise influenza viruses’ binding specificity previously; I thought then, and do now, that it is a very cool technology – and one that has shown in this case that H5N1 variants can be selected from an originally “wild” population, that preferentially bind the human-type receptor.
And they did it like this:
To examine the functional evolution of H5 HA receptor specificity in the laboratory, we implemented an in vitro receptor-binding virus enrichment approach that recapitulates in vivo selection. Synthetic 6′-sialyl (N-acetyl-lactosamine) (6′ SLN) was used as the affinity ligand mimicking the human receptor to capture spontaneous viral receptor variants on the surface of magnetic beads. Starting with a pool of 108 EID50 of A/Vietnam/1203/2004 (VN04 virus), we performed four consecutive rounds of in vitro binding and elution followed by isolation of 150 individual virus clones by plaque purification and characterization by sequence analysis.
No “genetic engineering” here – or furore over “killer viruses escaping the lab!” Possibly because (a) “mutant virus was transmitted by direct contact in the ferret model although not by airborne respiratory droplets”, and (b) “a reassortant virus with the mutant hemagglutinin, a human N2 neuraminidase and internal genes from an H5N1 virus was partially transmitted via respiratory droplets” [my emphasis].
Meaning they didn’t actually make anything that could immediately elicit such scare-mongering as the more notorious studies I and many others have reported on previously.
However, the grim NSABB folk were quick to decry the publication, saying “”I think it is fair to say that we would have liked to have seen it before it was published,” [Paul Keim, chairman of the National Science Advisory Board for Biosecurity], and the “…altered bird flu virus could mutate in dangerous ways if unleashed in nature”.
I am more worried, to be perfectly honest, over the dangerous ways the the wild type virus could mutate IN nature, given that mutants can be selected so apparently easily!