The truth about vine immunity

As the wine world becomes more aware of its environmental impact, it’s realising that the spraying needed to prevent fungal diseases is a problem. What’s the solution? One that’s often proposed has been boosting vine immunity. If we can get the vines to activate their immune system, say proponents of this theory, then they’ll become resistant and spraying won’t be needed. Healthy vines, suitably primed, can then fight off pests and diseases on their own. It’s why people talk about ‘boosting the immune system’ of plants through systems like biodynamics.

There’s a problem here. Plants don’t work this way.

How the system works

Understanding how plant immunity works has significant implications for how vineyards are managed, and also how viticulture can move towards less reliance on chemical interventions.

All organisms are fighting a constant war against infection. Both plants and humans share two ways of defending themselves. The first, common to both, is what’s called ‘innate’ immunity. These are the inbuilt, non-specific defences, that fight off attacks in a generalized sort of way. The first defence is a physical barrier: humans have skin, while plants have a waxy cuticle. But both humans and plants need to exchange gases with the atmosphere, and this creates a potential opening for bugs. Humans have the huge, warm, moist, more-or-less unprotected surface area of the lung, while plants have stomata, small openings to the outside, scattered on their surface. Some pathogens have found ways of getting through the physical barriers of skin and cuticles.

Another defence of innate immunity is the inbuilt ability to recognise the chemical signals used by pathogens. Humans have several different types of white blood cells whose job it is to recognise the danger signals and respond appropriately. Plants don’t have these types of circulating cells. Their first line of defence are receptors called pattern recognition receptors (PRRs), which sit on the outside of the cell membrane and recognise specific molecules. The signal from these receptors triggers a complex metabolic defence that, hopefully, stops further colonization of the plant tissue. This is called PAMP-triggered immunity, PTI (where PAMP stands for pathogen-associated molecular pattern).

Along with their innate defences, humans also have an adaptive immune system – and this is what’s responsible for the misunderstanding. Specialized white blood cells can learn to tell the difference between cells from their own body, and cells from outside, which creates an immune memory and allows the white blood cells to respond to specific threats. When someone gets sick, the adaptive immune system recognizes the bacteria or virus as “non-self” and starts to generate antibodies against it. When everything is going well, the resulting defence attacks the pathogen and then eliminates it from the body. Afterwards it keeps some memory of this attack, that will prevent a subsequent infection.

This system is the basis of vaccination. By injecting an inactivated bacteria or virus, or a fragment of one – along with an alarm signal called an adjuvant – medics are able to prime the adaptive immune system to make people resistant to infection by the real thing. The adaptive immune system is a remarkable, complex system, and its utility is highlighted by what happens when it goes wrong or is compromised.

Plants, however, have no such system.

Plant immunity

Plants don’t have an adaptive immune system, that can learn how to ward off invaders. They don’t even have immune cells. What they have are resistance genes (“R genes”), their next line of defence. Some pathogens produce molecules called ‘effectors’ that interfere in this initial PAMP-triggered immunity process, leaving the way free for them to invade the plant. This is when the second stage of plant immunity kicks in. Plants have a set of proteins that recognise a wide array of the effectors – the calling cards – released by the pathogens. As soon as they detect an attack, a process called effector-triggered immunity (ETI) kicks in. Paradoxically, this immune response doesn’t just kill the invader, it also kills the plant’s own cell. Called the hypersensitive response, this cell death stops the pathogen spreading. Plants can typically recognize around 1,000 different calling cards – but if a pathogen comes along that the plant doesn’t recognise, then it has no defence. It can’t create one, because it doesn’t have adaptive immunity. This means there is no way to “boost the immunity” of the vine. The plant can either defend itself, or it can’t.

But even when the plant has the right resistance genes, it’s still not certain of winning. Adaptable pathogens can stop the plant triggering its defences by developing new effector genes that the plant has no response for, or by acquiring new molecules that can suppress the plant’s response. In this case, the pathogen will win the battle.

Ways to protect the vine

Encounters between plant and pathogen can result in long-distance signals being sent to alert other parts of the plant or even neighbouring plants, to tell them to get ready. This process is called “induced resistance”, and it gets the cells elsewhere ready to respond. But it is only when the attack happens that the actual defences swing into action.

One potential way to boost vine defences may be by using compounds called “elicitors”. These are external signals that prime the defence responses. Work is currently underway to identify elicitors that can work in the grape vine, but despite promising lab results, results in vineyards have been disappointing.

There are two main pathogens affecting grape vines: Erysiphe necator (powdery mildew) and Plasmopara viticola (downy mildew). These are responsible for much of the spraying that takes place in vineyards worldwide – V. vinifera has no resistance to these American imports. Wild Vitis species in the USA do have resistance genes, though. For downy mildew, some 27 genes have been identified as potentially involved, and resistant varieties have been developed by breeding V. vinifera varieties with American species. Resistant vines that have been bred such as Regent and Cabernet Blanc have a gene called Rpv3 in them, that gives them resistance. Resistance to powdery mildew in hybrid vines has been shown to be due the R genes Run and Ren that have come from their American wild Vitis ancestry.

“In vineyards, the best way to avoid chemicals is to introduce new resistant cultivars which integrate at least two R genes against P. viticola and two others against U. necator,” says Dr Benoit Poinssot of the University of Bourgougne in Dijon. He has researched using elicitors to bump up the innate immunity in vines, but while this works in the greenhouse, it hasn’t been effective in the vineyard. And he advocates producing new vines with at least two resistance genes for each to avoid the development of resistance. This can come from either targeted breeding of new varieties, or through genetic modification – which is currently considered unacceptable by consumers.

Until then, vines will still be susceptible to these diseases, and growers will have to keep spraying their vineyards, with its attendant environmental impact.