Archive for the ‘biotechnology’ Category

Virology Africa 2015: Update and Registration

19 August, 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.


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.


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


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 – 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 –

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: or phone: +27 21 486 9111
Ms Deborah McTeer/Email: 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?



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.

Don’t fear GMOs – fear the hype!

31 July, 2015
I’m going to share a slightly disturbing exchange I just had with a dietician – because it shows that even well-educated people out there are buying into the anti-GMO frenzy.

And I will thank +Mary Mangan for pointing out some of the sites mentioned!

“Dear xxxx;

In answer to your statements and questions:

“For a while, I have had the suspicion that GMO foods might be related to the epidemic increase in allergies, worldwide”

Ummmm…there is no good evidence of a worldwide epidemic of allergies – like autism, there is better recognition of the state, rather than an increase in incidence.

“my two boys clinically react to GMO varients,”

WHICH variants?  Of what?  How do you know?  This is a dangerous path, and I have trod it with immunologists involved in this sort of research – the ONLY way you can say “it is due to a GM food” is if you have the EXACT equivalent that is NOT GM – and by that, I don’t mean “GM vs non-GM maize” – because that is not biologically equivalent unless you have the same exact variety.  The other way would be to isolate the proteins involved, and test them – which is not that difficult, and is something I have thought of doing, if only to settle this issue for once and for all.

I would strongly urge you…to look at the links I will list below: most people, and medics and non-plant scientists as well, really don’t understand what actually happens with modern GM.  What happens is that one or a very few genes are introduced into a plant, to make one or possibly two proteins – against the 40 000+ the plant already makes. The genetic modification is minimal compared to conventional or advanced breeding, which moves around whole chromosomes, and MUCH easier to track than use of irradiation, which is also used to change traits – and very often changes things you can’t see and therefore ignore, unlike GM techniques.

What is more, all of the changes induced in plants can be followed these days by techniques like whole genome sequencing and proteomics, so that we can genuinely put hand on heart and say “this is exactly equivalent to that, except for one protein”.  Seriously: the question of equivalence is no longer really up for discussion; it is subject to evidence – and I will point out that the standards expected for GM plants are FAR more stringent than for conventionally-bred plants, which may have far bigger changes in protein composition than any GM variety.

I hope this is helpful!



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.


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

Molecular evidence of Ebola Reston virus infection in Philippine bats

18 July, 2015

In 2008–09, evidence of Reston ebolavirus (RESTV) infection was found in domestic pigs and pig workers in the Philippines. With species of bats having been shown to be the cryptic reservoir of filoviruses elsewhere, the Philippine government, in conjunction with the Food and Agriculture Organization of the United Nations, assembled a multi-disciplinary and multi-institutional team to investigate Philippine bats as the possible reservoir of RESTV.

Sourced through from:

I recall at the time of its discovery, thinking that the virus must have reservoir species back home in the East – and that the fact that no disease had ever been reported from there in humans, meant it was completely under the radar.

There was also the issue that the virus seemed to have been transmitted between monkeys in the Reston facility without any direct contact – and even between rooms, which would imply airborne transmission.

Which frightened the cr@p out of many people, and I am sure especially those primate centre workers who were found to be seropositive for the virus, in the absence of any symptoms – even though at teh time, unsanitary conditions and overcrowding were blamed (

It is still something that needs to be looked at seriously: is Ebola Reston more transmissible than Zaire, Sudan and the rest – and if so, why?

Those interested can pick up on what happened at the time, here on the Ebola information pages I ran for a while:



See on Scoop.itPlant Molecular Farming

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.

Crystallising the tobacco mosaic virus

6 July, 2015

We saw last week how sulphur dioxide released from the Laki fissure system accounted for many deaths due to poisoning. We will stay with poisons this week as well, for virus has its roots in the Latin term for “poison”

Sourced through from:

Nice article – and from a newspaper in India, no less!  Adds to the history of virology in a very accessible way.

See on Scoop.itVirology News

Superbug threat prompts West to revisit Soviet-era virus therapy

4 July, 2015

Alarmed by rising resistance to antibiotics scientists and governments are taking a fresh look at bacteria-chomping viruses first isolated a century ago from the stools of patients recovering from

Sourced through from:

So nearly 100 years after Felix d’Herelle started championing phage therapy, the West is finally taking notice?  I’t actually way past time that they were taken seriously: the Eliava Institute in Georgia has nearly that long a history (d’Herelle influenced the founder to start their enormous collection of phages) of successful treatment of bacterial infections, but westerners have stayed wedded to increasingly ineffective antibiotics for the last 70-something years.

I know what I might work on in my old age….

See on Scoop.itVirology News


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