In 2016, the koala was upgraded from ‘Least Concern’ to ‘Vulnerable’ on the IUCN Red List of Threatened Species. The cuddly-looking marsupial is not only threatened by habitat loss, but also by disease – most notably chlamydia infections.
Different species of chlamydia bacteria infect koalas and humans. Previous research into the koala pathogen, Chlamydophila pecorum, shows something rather puzzling – not all koala populations are affected by the pathogen in the same way.
Infected koalas in the northern part of Australia have a higher rate of actual disease, while those in the south seem to either be less likely to be infected, or they do not show symptoms. Today, at the Microbiology Society’s Annual Conference, Dr Rachael Tarlinton from the University of Nottingham is presenting research that might explain why this is the case.
After a number of captive koalas across Australia died from diseases like lymphoma and leukaemia, an Australian wildlife vet called Dr Jon Hanger began searching for answers about why they were dying off in such numbers. One of the things he found was that koalas harboured a retrovirus within their DNA, opening the door to yet more questions.
Unlike a normal virus, which takes over its host’s cells, retroviruses operate by inserting themselves into their host’s genome. This means that when the host’s cells replicate, they are also making copies of the virus. For example, HIV – perhaps the most famous retrovirus – targets immune cells, rendering them unable to fight infections and making the infected person vulnerable to other, opportunistic pathogens.
Rachael and her colleagues wondered if the koala retrovirus (KoRV) could be the culprit for many premature koala deaths.
“At first, when we compared koalas from the north and south [of Australia], it looked like the southern animals were less likely to have the retrovirus,” says Rachael. “This led us to believe that the virus might have been making the northern population of koalas immunosuppressed.”
However, next generation sequencing methods showed that the animals thought to not carry the retrovirus did in fact have it. They simply had a version missing a large chunk of its genetic material.
Previous research had shown that KoRV was endogenous – the virus had worked its way into the koala’s sperm and ova cells at some point in history, making it able to be passed down from parent to offspring. Because of this, KoRV did not need the ability to be infectious anymore.
“Endogenous retroviruses can be missing large sections of genetic material because they don’t need it to replicate. They’ve inserted themselves into the host’s genomes and are copied along with the rest of it when the cell replicates,” explains Rachael. “This means that this virus isn’t a functional virus anymore, as it no longer has the parts it needs to make new copies of itself.”
Weirdly, endogenous, ‘defective’ viruses can actually protect the host animal from other infectious pathogens. It looks like KoRV may actually be protecting southern koalas from the infectious type of retroviruses, as well as diseases like chlamydiosis. Now, the questions for Rachael and her team are how, and why?
“Why do [the koalas’] genomes put up with these retroviruses for so long?” asks Rachael. “Do they do something beneficial for the host? Why doesn’t the genome kick them out? We will need to look at the differences between the retroviruses carried by both populations of koalas, and find out what they’re up to.
“If we can work out what the truncated virus is actually doing, there may be a potential opportunity to breed it back into the populations vulnerable to disease. This could have a massive impact on koala conservation, especially as they are being affected by habitat loss.”
Rachael will be presenting her work today at 17:15 in the ‘Regulation of RNA expression during virus infection’ session.