Tuesday, 31 July 2012

Info on the MMR scare

I'm not sure why there were some tweets about this today, since the article is over a year old, but this article explains how Dr. Andrew Wakefield "found" the "link" between MMR vaccine and autism, sparking the vaccination scare, and how Brian Deer, a journalist, exposed the fraudulent data behind the claims. Very good and interesting article. Apparently part of a series that I now must read!


Monday, 30 July 2012

Carrot (cup)Cake

I finally had some time to do some baking this weekend. I made my boyfriends' favourite . . .  carrot cake! Frosted with a cream cheese frosting and topped with crushed pecans and little candy carrots. The recipe I used is from Canadian Living (http://www.canadianliving.com/food/baking_and_desserts/canadas_best_carrot_cake_with_cream_cheese_icing.php/). I followed the recipe as is. Here are some tips: Definitely make sure you check the cake about 5 minutes early - mine was done then. You can omit the pecans if you want. For the pineapple, just drain the juice from the can - don't go overboard and try to squeeze all the juice out of the diced pineapple, it gets messy and takes some of the moisture away from the cake.
For the candy carrots, I use orange Starbursts and a green gel icing pen. Unwrap the Starbursts and place on a plate. Microwave them for about 3 seconds at a time until you can mould them, but they aren't melting. Cut each candy in half along the diagonal and mould them into a cone or carrot shape. Place on the top of the frosted cake and use the icing pen to add a stem to the carrot.
This recipe also works as cupcakes. It makes about 2 dozen (24) cupcakes.

Friday, 27 July 2012

GB Virus C – potential as an HIV therapeutic?

Today I read a paper and an opion piece from advance access for the journal Clinical Infectious Disease discussing GB virus C (GBVC) and its’ role in HIV infection. The opinion piece argued that GBVC should be used as a biovaccine in patients with HIV, because clinical data has demonstrated that those people coinfected with GBVC and HIV have a better prognosis than those with HIV alone.

GBVC infection is common and occurs worldwide. It is estimated that 1-5% of healthly blood donors in developed countries, and up to 20% in developing countries have replicating virus at the time of donation. GBVC has not been associated with any disease. In fact, blood donations are not screened for presence of GBVC because no known diseases occur in those that are infected.

GBVC infection has been associated with prolonged survival in HIV positive people, causing a 2.5 fold reduction in mortality during later (>5 years) stages of HIV infection. In addition, those people coinfected have higher CD4+ T cell counts, lower HIV viral load, delayed progression to AIDS, improved response to antiretroviral therapy, and reduced mother-to-child transmission.

The mechanism(s) used by GBVC to modulate HIV infection haven’t been fully elucidated, but appear to be numerous. GBVC infection alters the expression of HIV entry receptors, and causes the secretion of the natural proteins that bind to the receptors, making it very difficult for the virus to spread to uninfected cells. GBVC infects the same cells that HIV infects, and some of the proteins of GBVC are able to inhibit replication of HIV. Without replication, the virus is unable to make copies of itself, and spread throughout the body. Another protein from GBVC appears to directly interact with HIV, preventing the virus from entering new cells. Most of this should occur when GBVC is actively replicating. Once GBVC virus has been “cleared”, antibodies against the viral protein E2 appear. These antibodies can bind to either a cellular or viral target (it’s not known which) and prevent HIV entry into cells. GBVC is able to alter innate and adaptive immunity, which can help aid the anti-viral immune response to HIV infection. Combined, all of these effects of GBVC lead to improved prognosis for people with HIV infection.

The opinion piece makes a lot of valid points – if GBVC is harmless (and it certainly appears that way) then studies should be undertaken to determine if infecting HIV positive people with GBVC will be a successful therapeutic option. All the data so far points to yes.

For more information see:
Vahidnia et al. “Acquisition of GB Virus Type C and Lower Mortality in Patients With Advanced HIV Disease” Clinical Infectious Diseases

David Gretch “Advocating the Concept of GB Virus C Biotherapy Against AIDS” Clinical Infectious Disease

For lots of research and reviews, look up Jack T Stapleton 

Wednesday, 25 July 2012

An HIV cure is feasible?

Today, in Nature Reviews Immunology, The International AIDS Society (IAS) Scientific Working Group on HIV Cure published an opinion piece that summarizes their recommended key goals for the international community to establish a cure for HIV (http://www.nature.com/nri/journal/v12/n8/full/nri3262.html).

Combination, compliant use of antiretroviral drugs can improve the health and prolong life in HIV-infected individuals, and can reduce the rates of transmission. However, antiretroviral drugs do not fully restore health or normal immune status in patients – or eliminate the virus from their cells. In addition, only a minority of HIV+ people worldwide have access to antiretroviral therapy. Although the price of antiretroviral therapy has dropped, the cost of providing drugs to all 33+ million people infected with HIV for the rest of their lives is astronomical. But without treatment, the virus will be spread by those that remain untreated.

The IAS identified seven key priorities that will allow us to achieve a sterilizing (elimination of all HIV infected cells) or functional (lifelong control by immune system in absence of therapy, virus not completely eradicated) cure.

The key priorities are:
-       “determine the cellular and viral mechanisms that maintain HIV persistence during prolonged antiretroviral therapy and in rare natural controllers” – focus on establishment of latency, ongoing viral replication, homeostatic proliferations
-       “determine the tissue and cellular sources of persistent simian immunodeficiency virus or HIV in animal models and in individuals on long-term antiretroviral therapy”
-       “determine origins of immune activation and inflammation in the presence of antiretroviral therapy and their consequences for HIV or SIV persistence”
-       “determine host mechanisms that control HIV replication in the absence of therapy”
-       “study, compare and validate assays to measure persistent HIV infection and to detect latently infected cells”
-       “develop and test therapeutic agents or immunological strategies to safely eliminate latent infection in animal models and in individuals on antiretroviral therapy” – reverse latency, clear latently infected cells
-       “develop and test strategies to enhance the capacity of the host immune response to control active viral replication”

While these points are important, likely necessary to develop a cure, I wonder if we are anywhere close to answering these questions. Although a cure is sure to have the greatest impact on eradicating HIV, other issues also need to be addressed. Despite effective prevention options (condoms), 2.7 million people are infected with HIV each year. Alternative prevention strategies (Truvada, microbicides, vaccine) could lower transmission rates.  If you stop (or significantly lower) the spread, new infections can be prevented, which lowers the number of people that need treatment (or the cure, when developed). Preventing the spread of the virus should also be a focus, because there is no guarantee that everyone infected with HIV will receive the cure. This brings me to my second point, which is that many people (both those at “high risk” and those at “low risk”) do not know their HIV status. If a cure is developed, how do you ensure that everyone that is HIV+ receives it? Unless mandatory and regular testing of every single person is undertaken people that don’t want to get tested, or people who think they are “low risk” and have no need for testing, may continue to spread the virus. If the goal is an “AIDS free generation”, more than the science needs to be taken into consideration. 

Wednesday, 18 July 2012

Human Food Project

I recently started following PaleoDiet4Two on Twitter. They post about something called the Human Food Project, which aims to get a picture of the human microbiome. Today they have a post that is really interesting about the relationship between diet and cognitive function in the elderly. They tie this into the issue of school lunches. This is all based on a study that was published in Nature recently.

Check out the article (and learn more about the Human Food Project) here:


And go here for the original article from Nature:


Monday, 16 July 2012

HIV prevention drug approved by FDA

The FDA has approved the drug Truvada to prevent  HIV infection in adults who do not have HIV. The drug would be used (along with safe sex practices) by people whose partners are HIV positive to prevent transmission.

For more information . . .


and lots of news stories on Google News

Thursday, 12 July 2012

Fat and the Gut Microbiota

Our intestines contain millions of bacteria that help keep us healthy. They do a diverse range of things for us, and the gut microbiota (the total bacteria present) differs not only from person to person, but also differs based on the region that you live in . The gut microbiota of people that live here in North America will be drastically different than that of people from Asia, largely because our diets are very different. The North American diet tends to be high in fat. Little research has been done on the effects of a high fat diet on gut microbiota.

A study published last week in Nature found that dietary fat can alter the gut microbiota of mice, by changing the pool of bile acids. They compared diets high in milk fat and high in plant oils (unsaturated fat). Those mice that were fed a diet high in milk fat were still healthy, but had a change in their gut microbiota. If the mice were lacking an inflammatory signalling molecule called IL-10 they had an increased risk of developing colitis.

An introduction to the article:

The article:

Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice

Paleoanthropology - What did our ancestors eat?

Pretty cool article in Nature that is investigating what australopithecines ate by using proportion of stable isotopes of carbon contained in fossilized teeth.

An overview of the article:

And the article: