Agriculture Reference
In-Depth Information
continents (
Table 12.1)
. Some of these occur
commonly in the region and cause damaging po-
tato diseases; for example, contact and beetle
transmitted
Andean potato mottle virus
(APMoV)
and
Andean potato latent virus
(APLV). Others are
less widespread, for example
Potato virus T
(PVT),
rarely found, for example
Potato virus U
, or occur
only in wild potatoes, for example
Wild potato mo-
saic virus
. In addition, several are seedborne in
true potato seed and so are likely to spread when
true seed is exchanged between countries for
breeding purposes (e.g. Jones, 1981a, 1982a;
Valkonen
et al
., 1992; Valkonen, 2007). Al-
though quarantine regulations have apparently
avoided their establishment outside South Amer-
ica so far, vigilance needs to be maintained.
Pe -
pino mosaic virus
(PepMV) provides an example
where an indigenous virus from a
Solanum
spe-
cies (
Solanum muricatum
) growing in the Andean
region remained localized for >
25
years after its
initial detection in 1973. In 1999, it suddenly
appeared in Europe. PepMV then spread quickly
to most other continents (e.g. Jones
et al
., 1980;
Mumford and Jones, 2005; Jones, 2009). More-
over, among the common potato viruses, al-
though some important strains have already
spread outside the Andes, others may still do so,
including PVX resistance-breaking strain PVX
HB
(Moreira
et al
., 1980). The Y
N
strain of PVY pro-
vides a classic example of this kind of spread. It
was introduced into Europe inadvertently in po-
tato germplasm from the Andes about
55
years
ago (Todd, 1961; Brucher, 1969). It rapidly be-
came widespread and was soon introduced into
potato growing areas in other continents through
seed potato exports.
alterations in climate were likely to modify di-
verse components of viral disease in many differ-
ent ways, including viral pathogen geographic
ranges and relative abundance, rates of spread,
effectiveness of host resistances, physiology of
host-virus interactions, rate of virus evolution
and host adaptation, and effectiveness of control
measures. The complication of needing to con-
sider the effects of climate change parameters
on different vector types (e.g. the aphid, thrips,
whitefly, leafhopper, beetle, fungal and nema-
tode vectors of potato viruses) added a signifi-
cant additional variable. Another significant
variable arose from the need to consider the
likely effects of climate change parameters in in-
creasing the frequency of new encounters between
introduced crops and native plants, thereby ac-
celerating the emergence of new viruses caus-
ing potentially damaging infections (e.g. Jones,
2009; Navas-Castillo
et al
., 2011; Jones and Bar-
betti, 2012).
Overall effects at different latitudes
and altitudes
Depending on the type of pathosystem and cir-
cumstances, in many instances climate change
seems likely to enhance potato virus disease epi-
demics in higher latitude (temperate) regions.
Temperate potato growing regions likely to be af-
fected include ones in Canada, northern USA,
northern Europe, north-east Asia and southern
South America (Norse and Gommes, 2003; Jones
and Barbetti, 2012). Where potatoes are unirri-
gated, climate change is likely to have the opposite
effect in potato growing areas in drying mid-
latitude regions, for example parts of southern
Australia, Central America, the Middle East,
southern Europe, and North Africa. Potato-
infecting viruses best adapted to warmer regions
(e.g. GBNV,
Tomato chlorosis virus
(ToCV), TL-
CNDV, PLRV, PYMV, and
Potato yellow vein virus
(PYVV)) are likely to expand their geographical
ranges from the areas they currently occupy to
areas of higher latitude previously too cool for
them, and to formerly cooler higher elevations in
mountainous regions within the tropics or sub-
tropics. Conversely, the geographical distributions
of viruses adapted to cooler regions (e.g. APLV,
PVX, PVS, PVA, PMTV, and PVT) are projected to
12.2
Climate Change Predictions
The anticipated influences of climate change on
diverse aspects of plant viral pathogens, their
vectors, and the diseases they cause, have been
reviewed recently (Canto
et al
., 2009; Jones,
2009; Jones and Barbetti, 2012). Jones and Bar-
betti (2012) developed frameworks for (i) each
important direct and indirect climate change
parameter, and (ii) each significant biological
(host, vector, and pathogen) pathosystem param-
eter. These frameworks were then cross-checked
one against the other. This analysis revealed that
