Category Archives: Under the Microscope

Can cancer be contagious?

I doubt that many people would expect to be reading about cancer in an infectious disease blog, and yet here you are. Could it really be that I’m about to tell you that cancer, one of the most feared diseases in the developed world, can be contagious?

The answer is yes. That said, you don’t need to panic about a Hollywood-style infectious cancer outbreak just yet. Although there are examples of human cancers accidentally being transplanted into a new individual (1), these are rare and barely deserve being described as ‘infectious’. It could of course be argued that there are many viruses which can cause cancer (in fact, infectious agents are thought to cause 16.1% of cancers!), for example human papilloma virus which causes over 90% of cases of cervical cancers (2). However, in this case I am talking about cancers which are infectious in themselves.

The unfortunate animals affected are the cute-yet-ferocious tasmanian devils. Now only found on the island of Tasmania (an Australian state to the south of the mainland), the population of these carnivorous mammals has become endangered with thanks to a rampant infectious facial tumour.  The cancer is transmitted between individuals when they fight over food. The tumour grows and eventually prevents them from eating, starving them. For a long time it was not undertood how the cancer was able to spread – normally the immune system would recognise the cells that were from another individual and reject them (much like you often hear happening with transplants).  What is different this time?

A healthy Tasmanian devil Credit: arndbergmann
A healthy Tasmanian devil
Credit: arndbergmann

All normal cells express a class of molecule (known as MHCs) which lets the immune system know when a pathogen is in the cell. They are also the molecules which allow the immune system to spot foreign tissue, and are thereby the cause of transplant rejection. However, the cancerous cells don’t express these molecules, and so the immune system doesn’t respond to them (3). This means that when cancerous cells rub off onto another devil’s face, they are able to enter scratches and cuts and grow without being attacked by the immune system. Thankfully human cells are killed if they lack MHCs, so this should never evolve in human cancers.


  1.  Gartner et al., (N Engl J Med, 1996) Genetic Analysis of a Sarcoma Accidentally Transplanted from a Patient to a Surgeon
  2. Center for Disease Control and Prevention
  3. Siddle et al., (PNAS , 2013) Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer



Influenza: what’s in a name?

H1N1, H3N2, H1N7; we hear their names daily, but have you ever wondered what they mean? Why do we refer to the different strains of influenza by a ‘H’ and ‘N’ followed by a series of seemingly random numbers?

In order to replicate (reproduction is the ultimate ‘aim’ of all organisms!), viruses must first enter a host’s cell. In order to achieve this the virus must first interact with molecules on the host’s surface. These molecules must fit together like a lock and a key. If either one is the wrong shape, the virus won’t be able to enter the cell. As I described in ‘MERS CoV – will the Time-Bomb Explode?‘, this is especially important when looking at viruses which evolve to infect new species.

The letter ‘H’ stands for haemagglutinin, the ‘key’ on the virus. It binds to the ‘lock’ on the host cell, a molecule called sialic acid, and then enters. Interestingly, sialic acid is only found on animal lung cells, which is why we must inhale the virus to become infected!

The letter ‘N’ stands for neuraminidase. This is the ‘key’ which lets the virus back out of the cell. The virus needs to exit again so that it can go on to infect the next cell!

The haemagglutinin and neuraminidase proteins can vary, and each strain of virus will have one type of each. The number of each has been allocated purely based on the order in which it was discovered, so H1N1 has the first haemagglutinin and first neuraminidase proteins to be discovered.

That’s all very well, but why name a virus after these two proteins? The reason is that these proteins are the proteins that can most easily be ‘seen’ by the host’s immune system. Antibodies are made against these proteins, and this is what allows for the creation of immunity. That’s why being infected with H2N7 won’t protect you against H3N2 infection, and why scientists have to make informed guesses as to which strains should be vaccinated against in any one year.