Animals such as rats are often regarded as disease carriers. But when it comes to the spreading of illnesses, it turns out other animals have more reason to fear us than we them.

An analysis of viral genomes has found that when viruses move between humans and other animals, in 64 per cent of cases it is humans infecting other animals – rather than the reverse.

“We give more viruses to animals than they give to us,” says at University College London. For instance, after the SARS-CoV-2 virus jumped from bats to humans, possibly via another species, humans passed it on to many other species.

Tan and his colleagues have been using a global database of sequenced viruses to study how they jump between species. There are nearly 12 million sequences in the database, but many are incomplete or lack data on when they were collected and from what host species.

So the researchers narrowed down the 12 million to roughly 60,000 high quality sequences with full accompanying data. They then created “family trees” for related viruses.

Altogether, they identified nearly 13,000 viral lineages and 3000 jumps between species. Of the 599 jumps involving humans, most were from humans to other animals rather than vice versa.

The team wasn’t expecting this, but in retrospect it makes sense, says Tan. “Our population size is huge. And our global distribution is basically everywhere.”

In other words, a virus spreading among humans will have numerous opportunities to jump to many other species all around the world, whereas a virus circulating in a non-human species that is limited to one region will have far fewer opportunities.

SARS-CoV-2, MERS-CoV and flu viruses were those most commonly passed to other animals via humans, the study found. This is in line with other studies showing, for instance, that SARS-CoV-2 has spread from people to pets, zoo animals, farmed animals such as mink and to wild animals such as white-tailed deer.

However, even when SARS-CoV-2, MERS-CoV and flu viruses were excluded from the analysis, the team found that 54 per cent of jumps were from humans to other animals.

The spread of viruses from humans to other species is a threat to many endangered animals, says Tan. For instance, several wild chimpanzees have died in Uganda due to outbreaks of human metapneumovirus and human respirovirus.

An antibody therapy could treat infections caused by a dangerous strain of bacteria that most antibiotics can’t kill. While the treatment hasn’t been tested in humans yet, it is effective in mice.

Methicillin-resistant Staphylococcus aureus (MRSA) is one of the deadliest bacteria. It killed more than 100,000 people worldwide in 2019 and has evolved to evade all but seven antibiotics.

“One of the challenges in treating [MRSA] is that the organism is very good at escaping different immune responses,” says at NYU Langone Health in New York. This includes the body’s deployment of proteins known as antibodies, which identify and attack pathogens.

Torres and his team developed a treatment by introducing genetic mutations to a human antibody that attacks MRSA. They engineered small proteins called centyrins onto the molecule’s surface – these prevent bacteria from drilling holes into immune cells. The engineered antibody targets 10 disease-causing mechanisms of MRSA.

To test its efficacy, the researchers gave antibody infusions to 20 mice 4 hours after they were infected with MRSA. Half the mice received infusions with the new antibody treatment while the other half received antibodies ineffective against the bacteria.

After three days, skin lesions in the mice treated with engineered antibodies were, on average, 95 per cent smaller than those seen in the control group. They also had an average of 98 per cent fewer bacteria in infected tissues than untreated animals, indicating the treatment can clear MRSA infections that progress to other organ systems.

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The team conducted a separate experiment in 54 mice with MRSA-induced kidney infections and found that the antibody treatment boosted the efficacy of vancomycin, one of the so-called “last resort” antibiotics. Mice on the combination therapy had 99 per cent less bacteria in kidney tissue than mice treated with vancomycin alone.

“Even if [this] product were to fail to reach efficacy endpoints in human clinical trials, it’s a significant step forward,” says at Vanderbilt University Medical Center in Tennessee. That is because it offers a new blueprint for designing antibody therapeutics, he says.

“The number of [effective] antibiotics has been shrinking and shrinking and shrinking,” says Torres. “So, the importance of this research is to provide a new option, or at least a new pathway whereby we can generate new treatments to prevent death and infections.”