Archive for the ‘Vaccines: General’ Category

Virology Africa 2015: Update and Registration

19 August, 2015

REGISTRATION IS NOW OPEN – VIROLOGY AFRICA 2015

On behalf of the Institute of Infectious Disease and Molecular Medicine of the University of Cape Town and the Poliomyelitis Research Foundation, we are pleased to invite you to Virology Africa 2015 at the Cape Town Waterfront.

VENUE AND DATES:

The conference will run from Tuesday 1st – Thursday 3rd December 2015. The conference venue is the Radisson Blu Hotel with a magnificent view of the ocean. The hotel school next door will host the cocktail party on the Monday night 30th November and in keeping with Virology Africa tradition, the dinner venue is the Two Oceans Aquarium.

IMPORTANT DATES

Early Bird Registration closes – 30 September 2015
Abstract Submissions deadline – 30 September 2015

The ACADEMIC PROGRAMME will include plenary-type presentations from internationally recognised speakers. We wish to emphasise that this is intended as a general virology conference – which means we will welcome plant, human, animal and bacterial virology contributions. The venue will allow for parallel workshops of oral presentations. There will also be poster sessions. Senior students will be encouraged to present their research. We have sponsorship for students to attend the meeting and details will be announced later in the year.

A program outline has been added to the website

WORKSHOPS

Our preliminary programme includes two workshops.

There is a hands-on workshop on “Plant cell packs for transient expression: Innovating the field of molecular biopharming”, with the contact person being Dr Inga Hitzeroth – Inga.Hitzeroth@uct.ac.za. This workshop will run at UCT one day before the conference, 30th November, and a second day, 4th December, after the conference.

The second workshop is on “”Viromics for virus discovery and viral community analysis”. The workshop at UCT will be on 4 and 5 December with the contact person being Dr Tracy Meiring – tracy.meiring@uct.ac.za.

Some of the workshop presenters will be integrated into the conference programme but the practical components will be run at University of Cape Town. Separate applications are necessary for each workshop.

If you are prepared to fund an internationally recognised scientist to speak at the conference or if you wish to organise a specialist workshop as part of the conference, please contact
Anna-Lise Williamson or Ed Rybicki.

For any enquiries please contact
Miss Bridget Petersen/ Email: conference1@onscreenav.co.za or phone: +27 21 486 9111
Ms Deborah McTeer/Email: conference@onscreenav.co.za or +27 83 457 1975

Laurie Garrett on Ebola: the recent history

18 August, 2015

20 years after I first posted something by Laurie Garrett – who has written two of the the most thought-provoking, informative and frightening books I have ever read (The Coming Plague, and Betrayal of Trust) – I see she has just published possibly the single best account of the recent Ebola virus disease outbreak in West Africa.

Seriously.  Exhaustive, deep, analytical – and like her books, throwing some harsh light on world health care systems (or the lack thereof, in the case of the WHO), while at the same time making useful suggestions.

Like this one:

“And so it comes back to money. The world will get what it pays for—and right now, that is not very much.”

Absolutely: consider that the late and haphazard and meagre response by most governments let the epidemic peak and then start to subside – without actually, in the case of the US, managing to get more than one treatment centre functional in Liberia, before they ran out of patients.  That the health systems of all three countries are in such bad shape that they can’t deal with childbirth and malaria right now.

Laurie, it’s a great piece, really it is. It’s also depressing as hell.  But that’s life!

How should we preserve old viruses?

12 August, 2015

I was reminded via Twitter by Vincent Racaniello, he of “virology blog” fame, of the problem of preserving stocks of old viruses.

Particularly, in his case, of stocks of a virus that may be eradicated in the wild in a few years, and then – according to him – will need to be destroyed.

Surely we need to at least preserve sequence information of these pathogens before we let them go into oblivion, the way variola and rinderpest viruses have already gone?

So I wrote this to him:

“Great that you have preserved these samples – but a longer-term strategy needs to be adopted, before completely irreplaceable specimens are lost forever, to you and to science in general.

tmv sedimI have the same problem: a colleagues’ samples of plant viruses; beautifully preserved in heat-sealed glass vials, dried over silica gel, dating back in some cases to the early 1960s. For that matter, I have about a thousand glass bottles of liquid plant virus samples at 4degC, dating back in some cases over 40 years – and still viable.

Surely there is a case to be made for preserving some of these viruses? Mining them for sequence in this metagenomic age is not that difficult; preserving their infectivity, however – another matter. Some of my plant viruses are probably bomb-proof; your poliovirus samples, on the other hand – probably slowly deteriorating as we watch.

A wider conversation is needed: I know of other archives, of old poxvirus collections for example, that will be lost forever in a few years. Should we not get an international effort going to log them, sequence them, preserve them?

I think so.

Want to join in?

Yours,

Ed”

If any of you out there have a similar problem, let’s hear from you – and maybe we can do something to at least preserve the genetic information in unique collections.

Anyone interested? A candidate virology textbook…

28 July, 2015

I would like to test the response to a Introduction to Virology ebook that I want to develop from my extant Web-based material, given that this is likely to disappear soon with our Web renewal project here at UCT.

Virus_Picture_Book_copy_iba

Download the Virus Picture Book excerpt here. And then please tell me what you think / whether you would buy one (projected price US$15 – 20)?  Ta!

Ebola on the Web – 20 years on

21 July, 2015

I have already done a partial retrospective on having been reporting on Ebola haemorrhagic fever viruses for just over 20 years – but I totally forgot to commemorate that I have been producing Web pages for just over 21! So I’m going to go on a nostalgic ramble through the past, mainly using Ebola as the vehicle, and highlighting some of the history of virology along the way.

By the way, I HAVE to commend the Wayback Machine here: I have also previously bemoaned the fact that Web pages are NEVER preserved by their creators at regular intervals – but this is exactly what they do.  From 1997 onwards in the case of the whole of the University of Cape Town’s site and mine as part of that – and how interesting it has been to go back and look at what I thought was cool then!  But actually, what’s not to like? I mean, there’s hepatitis G, Congo fever, smallpox, Ebola, “equine morbillivirus” (aka Hendra virus) – and life on Mars. Or not B-)

What’s interesting, though, is that they have preserved almost all of my Ebola news pages – dating from May 1995, from right near the onset of the Kikwit Ebola epidemic.  There’s all sorts of interesting stuff there – though with some holes, caused by Lost Pages – ranging from a discussion of the possibility of finding Ebola in cotton plants [not!], with my old friend Murilo Zerbini, to a thread on “Candidate for the Ebola Reservoir Organism” from the late lamented bionet.virology discussion group, to whether Ebola Reston was airborne (probably not).

Great historical stuff, right there – and thank deities it is preserved via Wayback, because our upcoming Web renewal project here at UCT will kill ALL links from our Departmental site.  Get it while you can!

And while we’re at it: here’s a useful list of all Ebola-related posts on ViroBlogy since 2011.  Note when the first mention of plant-made antibodies to Ebola virus was….

Molecular evidence of Ebola Reston virus infection in Philippine bats

18 July, 2015

The Discovery of Filoviruses

Ebola virus mutating, scientists say

29 January, 2015

First Ebola case linked to bat play – really?

30 December, 2014

Ethical dilemma for Ebola drug trials

13 November, 2014

Rabies Vaccine Protects Nonhuman Primates against Deadly Ebola Virus

26 October, 2014

Packs of wild dogs spread Ebola after eating corpses!! Or…not, maybe?

13 October, 2014

Norway to get world’s last dose of ZMapp – update

8 October, 2014

8 September, 2014

20 years on, and here we are with Ebola, again

25 August, 2014

5 Viruses That Are More Frightening Than Ebola

20 August, 2014

What Would Happen if You Got Ebola?

13 August, 2014

Plant-made antibodies used as therapy for Ebola in humans: post-exposure prophylaxis goes green!

5 August, 2014

Has the Time Come to Test Experimental Ebola Vaccines?

30 July, 2014

Plant-Based Antibodies, Vaccines and Biologics 5, Part 5

3 September, 2013

Ebola Outbreak in Uganda: CDC Rushes to Contain Virus

8 August, 2012

More Ugandans Admitted with Possible Ebola

1 August, 2012

Ebola reaches Uganda’s capital

31 July, 2012

31 July, 2012

Canadian researchers thwart Ebola virus

14 June, 2012

African monkey meat that could be behind the next HIV

25 May, 2012

Current Opinion in Virology – Mass extinctions, biodiversity and mitochondrial function: are bats ‘special’ as reservoirs for emerging viruses?

5 April, 2012

When dinner could kill you: smoked chimpanzee, anyone?

14 January, 2012

Virology Africa 2011: viruses at the V&A Waterfront 2

19 December, 2011

Ebola: ex tobacco, semper a vaccine novi

6 December, 2011

Influenza virus: a short introduction

14 July, 2015

This is excerpted from the ebook “Influenza Virus. Introduction to a Killer”, which is available here for US$9.99 .

Influenza: the disease

Influenza: a disease and a virus

Influenza as a disease in humans has been known for centuries; however, its cause was only discovered in the early 20th century: this was the group of viruses now known as Influenza virus types A, B and C.

There are several influenza viruses circulating in humans at any one time; these cause “seasonal flu”, which is usually a mild disease because most people have some degree of immunity.

Influenza pandemics, however, are caused by novel viruses – which are generally derived from animals, and usually originate in birds.  Here, the disease can be much more severe.

Influenza viruses have caused some of the biggest and yet some of the most insidious disease outbreaks to have hit humankind: from 1918 to 1920, the “Spanish Flu” pandemic killed more than 60 million people across the world; subsequent pandemics in 1957, 1968 and 1977 killed millions more, and the count is still unclear on the 2009 pandemic. However, in any given year more than 400 000 people probably die of so-called “seasonal flu” – yet universal vaccination against it is still a dream.

What is Influenza?

What is Influenza?

The Centers for Disease Control and Prevention in the USA define influenza as

“…a contagious respiratory illness caused by influenza viruses that infect the nose, throat, and lungs. It can cause mild to severe illness, and at times can lead to death.”

The disease is transmitted mainly via droplets of respiratory secretions: these result from sneezing or coughing, which blows out a fine cloud of droplets or aerosol from the upper airways of infected people.  Breathing in or inhalation of these droplets – which can happen from 2 metres away – or transfer of droplets by hand from a contaminated surface to the mouth, is enough to cause infection. 

The virus initially infects cells of the upper airway, or the respiratory epithelium.  Spread to lower parts of the respiratory system, such as into the lung, depends upon the particular virus, and whether or not the individual is partially immune.

  • Fever or chills
  • Cough
  • Sore throat
  • Rhinitis, or runny nose
  • Muscle or body aches, headaches
  • Tiredness, “fuzzy head”
  • Vomiting and/or diarrhoea (more common in children than adults).

The average incubation period, or time from infection to disease, is about 48 hours.  Full recovery can take a month, although about two weeks is more common in seasonal flu.  People can pass on the virus before they show symptoms, and each infected person on average infects another 1.4 people.

While flu may be mild enough that it is hardly noticed, severe disease can also occur – especially in the elderly, the very young, heavy smokers, people who are chronically ill from other causes – and immunocompromised individuals.

While the virus can cause pneumonia directly due to damaging lung tissue, as happened in the “Spanish Flu” pandemic, severe illness with pneumonia is more usually due to secondary bacterial infections – which can be treated with antibiotics, unlike the viral pneumonia

Seasonal flu, or the disease caused by viruses circulating in the population, typically has an “attack rate” of between 5-15% of the population in annual epidemics.  Case fatality rates, or deaths among those infected, are usually between 0.1 – 0.3%. However,  pandemic flu – caused by new strains which arise spontaneously, and to which people are not immune – can attack from 25-50%, and kill 5% of those infected.  Seasonal flu also mainly infects children – because older people are often immune – but mainly causes severe disease and death in the elderly: up to 90% of victims are usually 65 or older

Conversely, pandemic strains may affect a different set of age groups: for example, the Spanish Flu affected mainly healthy young adults.

Seasonal influenza is typically a disease of the autumn and winter seasons in temperate zones – meaning October – March in the northern hemisphere, and April – August in the southern.  The CDC FluView graph shown here clearly illustrates the cyclical nature of seasonal flu, tracked in the USA over a 5 year period.  However, the exact timing is not reliable, and epidemics may peak as early as October in the north, or April in the south, or as late as the end of the season.

Tropical zones have a different epidemic profile:

here the virus may circulate year-round, typically with a peak during the one or two rainy seasons.  Because of demographic reasons incidence is severely under-reported: however, in a seasonal outbreak in Madagascar in 2002, there were more than 27 000 cases reported in 3 months, with over 800 deaths for a case-fatality rate of around 3%.  A WHO coordinated investigation of this outbreak found that there were severe health consequences in poorly nourished populations with limited access to adequate health care.

Why is influenza seasonal?

Many reasons have been invoked over the years to explain this, ranging from temperature, humidity, school schedules, increased indoor crowding during winter or rainy seasons, and even variations in host immunity due to lack of vitamin D or melatonin.  However, the same reasons cannot be given for both the increase in influenza incidence in temperate climates with the onset of winter, and the rainy season peaks in tropical regions, given the very different environmental conditions prevailing.

A recent study set out to systematically determine the interactions between relative humidity, and salt and mucus and protein content of droplets containing live flu virus, on the viability of the virus – and came up with conclusions that could explain the temperate / tropical transmission differences.

Essentially, their explanation for temperate region seasonality is that there is low relative humidity indoors in winter due to heating: this leads to increased survival of virus due to drying of particles – influenza A viruses are stabilised by being dried in the presence of salts, mucus and proteins – and leads to aerosols persisting longer in the interior environment due to smaller size, and being propagated further, meaning most transmission would be by this route.  Increased time spent indoors and increased indoor crowding due to the climate would obviously increase transmission rates under these conditions. 

Tropical environments present a very different picture: here, high temperatures would accelerate virion decay, which would tend to decrease any transmission.  However, in rainy seasons, temperatures drop and relative humidity increases to nearly 100% – conditions conducive to survival of large drops, which settle out quickly onto surfaces, where the virus remains viable.  Thus, transmission could be mainly by surface contact.  The same social factors apply as for temperate climates, with frequent rain leading to more time indoors and more crowding – and a greater opportunity for transmission.

The guru speaks: new eBooks on viruses!

24 June, 2015

I have to thank my long-time digital media guru, Alan J Cann, for reviewing our humble eBook offerings in MicrobiologyBytes.  You good man!  Much appreciated, and it will not have escaped our attention that this endorsement may actually result in sales.  If so, a glass or three of the finest red is yours if you come to these shores, good sir B-)

eBook on “Influenza Virus: Introduction to a Killer”

17 June, 2015

For some five years now, I have been simultaneously writing two ebooks on viruses. The one – originally part of a longer effort not yet finished – is “A Short History of the Discovery of Viruses” which is also advertised on Virology News; the other is a labour of love on influenza.

Labour of love for me because I got more into it the more I read, and because Russell Kightley’s images were so amazing.

Both were written using Apple’s iBooks Author app; both are designed to be read by Apple’s iBooks app on iPad, iPhone or Mac.

So here it is:

Influenza Virus: Introduction to a Killer

Enjoy. Buy!

Influenza_1-6-15_sample_iba

 

Tracing the bird flu outbreak in North American poultry flocks

14 May, 2015

(Reuters) – The United States is facing its worst outbreak on record of avian influenza as three deadly strains have hit North American poultry flocks since December, with the spread of infection picking

Source: www.reuters.com

Useful timeline!

See on Scoop.itVirology News

Viruses and Human Cancer: The Molecular Age

1 April, 2015

Hepatitis C virus

A suspicion that other viruses were involved in post-transfusion-(PTF) related hepatitis was first aired by Harvey J Alter and colleagues, after proof in 1972 that some PTF-related hepatitis cases had no HBV antigen associated with them.  By 1977 hepatitis A virus (HAV, infectious hepatitis) had been excluded as well, and the term “non-A, non-B” hepatitis (NANB) was coined.  By 1978, transmission studies using human serum injected into chimpanzees showed that

“Hepatitis was transmitted by serum derived from patients with chronic as well as acute hepatitis, strongly suggesting a chronic carrier state for the agent responsible for non-A, non-B hepatitis. Non-A, non-B hepatitis thus seems to be due to a transmissible agent which can persist and remain infectious for long periods”.

There was also evidence from Japan the same year that there might be a novel antigen – hepatitis C (HC) antigen – associated with NANB PTF hepatitis.  In 1979, it was suggested from ultrastructural studies in cells from infected chimpanzees that more than one NANB agent might exist; by 1980 Alter had concluded that that the NANB hepatitis agent(s) played a dominant role in the pathogenesis of PTF hepatitis. In 1987, in an interesting application of essentially the same technology used to characterise the first viruses, Alter’s group used polycarbonate membranes to filter the infectious agent, and showed it was  30-60 nm in diameter, and therefore highly unlikely to be a retrovirus, as had been suggested by some.

Also in 1987, Michael Houghton, Qui-Lim Choo, and George Kuo at Chiron Corporation collaborated with  DW Bradley at the CDC in using the much newer technology of constructing a random-primed cDNA clonal library from RNA extracted from human plasma in a lambda phage expression vector, and screening proteins expressed from the library against NANB hepatitis-infected patient serum.  They discovered one sequence that produced a protein fragment that bound antibodies, sequenced it, and used the sequence to “primer walk” through the entire genome by repeated cDNA generation, cloning and sequencing.  They published their finding in 1989 of

“…an RNA molecule present in NANBH infections that consists of at least 10,000 nucleotides and that is positive-stranded with respect to the encoded NANBH antigen. These data indicate that this clone is derived from the genome of the NANBH agent and are consistent with the agent being similar to the togaviridae or flaviviridae”.

The agent was unique among viruses characterised until then, as no virus particle had yet been seen, let alone isolated. Alter and his team meanwhile tested for the presence of the virus in NANB patient samples, and in 1989 also published a paper – back-to-back with the previous – on

“An assay for circulating antibodies to a major etiologic virus of human non-A, non-B hepatitis”.

The sequence of the putative agent allowed cloning and expression of a putative capsid protein in yeast, which allowed large-scale screening of patient samples and donated blood.  From their paper:

“These data indicate that HCV is a major cause of NANBH throughout the world”.

There was also already evidence that NANBH was associated with hepatocellular carcinoma (HCC) in Japan: M Sakamoto and colleagues showed that 90% of HBsAg-seronegative patients, who were also overwhelmingly HBV DNA-negative, showed evidence of chronic hepatitis in the non-cancerous liver, and 29% had a history of blood transfusion. This was followed as early as 1989 by evidence that 65% Italian HCC patients had antibodies to HCV, and again the same year by evidence from Spain that 75% of HCC patients had HCV antibodies, which

“…indicate[s] that HCV infection may have a role in the pathogenesis of hepatocellular carcinoma, even in patients with chronic liver disease apparently related to other agents such as alcohol”.

By 1990, K Kiyosawa and colleagues felt able to state that:

“These data suggest the slow, sequential progression from acute hepatitis C virus-related non-A, non-B hepatitis through chronic hepatitis and cirrhosis to hepatocellular carcinoma and support a causal association between hepatitis C virus and hepatocellular carcinoma”.

These findings rapidly led to the revelations that hepatitis C virus (HCV) was implicated in both an acute and relatively mild illness that lasts only a few weeks, and a chronic form that is usually more serious and can last lifelong.  Between 15–45% of infected persons spontaneously clear the virus within 6 months; however, the remaining 55–85% will develop chronic HCV infection.

Up to 150 million people globally are chronically infected with HCV.  Moreover – also from the WHO site – a significant number of these people will develop liver cirrhosis or liver cancer, and up to 500 000 people die worldwide every year from HCV-related liver disease.

There is as yet no vaccine against HCV infection, although trials are quite far advanced – and one candidate combination prime-boost strategy from Eleanor Barnes and coworkers seemed to show promise as of the end of 2014.  This consisted of

“…a replicative defective simian adenoviral vector (ChAd3) and modified vaccinia Ankara (MVA) vector encoding the NS3, NS4, NS5A, and NS5B proteins of HCV genotype 1b” – which is using two well-characterised viruses as gene vectors to combat a third.

The authors make the point that the responses they achieved in human volunteers are similar to those seen in people who control natural infections.

Meanwhile, chemotherapy for chronic infections is both a realistic and well-established area: there are a number of treatments on the market already, and there have been significant recent developments which may make treatment even more effective.

HCV particles were finally characterised from cell culture-grown virus: both enveloped and non-enveloped pleomorphic spherical particles were found, of around 60 nm and 45 nm in diameter respectively.  This agrees well with the estimation by filtration of 30-60 nm previously determined in 1987.  The virus is classified as a ss(+)RNA genome flavivirus, similar to yellow fever virus, in the genus Hepacivirus, family Flaviviridae

Kaposi sarcoma herpesvirus

Moritz Kaposi in 1872 described what was originally called an “idiopathic multiple pigmented sarcoma of the skin”, which present as

“…disseminated blood- or bruise-coloured skin lesions (flat plaques or nodules) in the skin, usually on the lower extremities though sometimes on the hands and arms”.

What was subsequently called Kaposi Sarcoma, or KS, was at first thought to occur only among elderly men of Jewish, Arabic or Mediterranean origin; however by the 1950s it was realised it was quite common in sub-Saharan Africa, which led to the first suggestions that it might be caused by a virus.

In 1981-1982, however, the CDC received reports of KS occurring in otherwise healthy young homosexual men in California – often together with Pneumocystis carinii pneumonia, which was also previously very rare.  The disease was also much more aggressive, and spread beyond the skin into other tissues including bone, the mouth, gastrointestinal tract and lungs.

While there was at this time still no clue as to why this should be, the link to sexual acts as well as the previous observation that KS occasionally appeared in immune-suppressed organ transplant patients, led epidemiologists to discover the sexual transmission of immunodeficiency that led to the discovery of HIV and its causation of AIDS.

Valerie Beral and colleagues working at the CDC in the late 1980s used epidemiological data on KS in AIDS patients to build a compelling case for the tumour being caused by another sexually transmitted virus.  In a landmark paper in The Lancet, they announced in 1990, on the basis of painstaking and traditional-style investigation of 8 years’ worth of information from more than 90 000 people with AIDS collected in the US by the CDC since 1981, that:

“In the United States Kaposi’s sarcoma is at least 20000 times more common in persons with [AIDS] than in the general population and 300 times more common than in other immunosuppressed groups…Kaposi’s sarcoma was commoner among those who had acquired the human immunodeficiency virus (HIV) by sexual contact than parenterally, the percentage with Kaposi’s sarcoma ranging from 1% in men with haemophilia to 21% in homosexual or bisexual men. Women were more likely to have Kaposi’s sarcoma if their partners were bisexual men rather than intravenous drug users”.

The UK Cancer Research site on KS has an excellent account of the study as well as of its impact – one aspect of which was the proof in 1994 that indeed a virus was involved, using modern.  This was published by Y Chang and colleagues in Science, and detailed the use of the very modern technique of:

“Representational difference analysis … to isolate unique sequences present in more than 90 percent of Kaposi’s sarcoma (KS) tissues obtained from patients with acquired immunodeficiency syndrome (AIDS). These sequences were not present in tissue DNA from non-AIDS patients, but were present in 15 percent of non-KS tissue DNA samples from AIDS patients. The sequences are homologous to, but distinct from, capsid and tegument protein genes of the Gammaherpesvirinae, herpesvirus saimiri and Epstein-Barr virus. These KS-associated herpesvirus-like (KSHV) sequences appear to define a new human herpesvirus.”

This became human herpesvirus 8 (HHV-8), the newest of the seven viruses known to cause human cancers.

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