The epidemiological landscape of viral diarrhea in pigs has shifted fundamentally over the past two to three years. If you still respond using the old framework of “preventing PEDV in winter, administering classical vaccines, and using feedback when disease occurs,” you may unknowingly fall into several of the biggest control blind spots today.
According to monitoring data from 2025–2026, the most noteworthy changes are concentrated in three areas: PEDV has completed a strain replacement from classical G1 to G2c, and G2c carries clear immune-escape mutations; the detection rate of rotavirus (PoRV) has surpassed that of PEDV, making it the most frequently detected diarrhea pathogen; and mixed infections of PEDV and PoRV have replaced the PEDV-TGEV combination as the most prevalent type of mixed infection in diarrhea cases. Taken together, these three changes mean that the strategy of “administering one classical vaccine and waiting for winter to pass” is systematically failing.
I. PEDV: G2c has become overwhelmingly dominant, and the neutralizing antibodies induced by classical vaccines “cannot reach it”
PEDV genotype replacement is currently the most critical variable. Analysis of 69 S gene sequences covering 9 provinces, including Anhui, Guangxi, and Hebei, in 2021—2024 showed that the G2c subtype accounted for as much as 69.57% of outbreak strains (48/69). The once-dominant G2a (20.29%) and G2b (2.89%) have contracted sharply, while the S-INDEL recombinant type accounted for only 7.25%. Another study of the current outbreak group likewise confirmed that G2c variants accounted for close to seventy percent of circulating strains. G2c has already established its dominance among PEDV strains in domestic pig populations. This is not a trend that is “emerging”; it is a reality that has already taken hold.
The reason G2c merits separate discussion is not that its name is new, but that it carries molecular features capable of substantially weakening the protection provided by existing vaccines. The S protein is the main target of PEDV-induced neutralizing antibodies. G2c has multiple characteristic amino acid substitutions in the S1 and S2 regions, including N139D, Y182H, I287M, F345L, and L998M. Structural modeling shows that these substitutions are not “silent”; they cause significant changes in local conformation—N139D converts a random coil into an α-helix, I287M and F345L alter the conformation of the receptor-binding interface, and L998M induces α-helix extension near the fusion peptide. These conformational “reshapings” directly impair the efficiency with which antibodies induced by conventional vaccines recognize G2c strains.
Neutralization assay data quantify this impairment. Using a representative G2c strain as the target, the geometric mean neutralizing titer (GMT) was only 10 in the group given a CV777 (G1a) live vaccine followed by an inactivated booster; it was only 20 in the group given two doses of AJ1102 (G2b) inactivated vaccine, and just 40 in the group given an AJ1102 live vaccine followed by an inactivated booster. Meanwhile, G2c strains are highly virulent in newborn piglets: following inoculation with the AHCZ02 strain, the piglets reached 100% mortality within 66 hours, accompanied by severe watery diarrhea, rapid dehydration, and severe jejunal villous atrophy. There is a gap between the antibody levels induced by classic vaccines and the actual pathogenicity of G2c that is difficult to bridge by “giving one additional booster.”
The national PEDV detection rate reached 70.75% in 2025. Although it fell to 28.1% in the first quarter of 2026, the reported number of PED cases and deaths remained the highest among Category II animal diseases. Short-term fluctuations in the detection rate do not change one basic assessment: PEDV continues to circulate, and the dominant strain has changed to one that classic vaccines cannot effectively cover.
Two. Rotavirus: Detection rate surpasses PEDV, becoming the “number-one pathogen by volume”
If the problem with PEDV is that “the strains have changed,” then the problem with rotavirus is that “its scale has changed.”
Monitoring data for 2025 show that the positivity rate for PoRV reached 75.65%, exceeding PEDV’s 61.33%; by the first quarter of 2026, the PoRV detection rate had climbed further to 94.6%, reaching as high as 97.9% in some regions with a high incidence of diarrhea. In East China and Central China, the PoRV detection rates reached 90.2% and 97.9%, respectively, forming an endemic background with a high pathogen load year-round.
The clinical profile of PoRV needs to be recalibrated. When it occurs on its own, its mortality rate is usually lower than that of PEDV, but its morbidity rate is very high, and it mainly affects piglets aged 2–8 weeks, especially those around weaning. Clinically, it is characterized mainly by yellow or white pasty diarrhea. The disease course is relatively mild, but it can easily lead to stunted growth and runting. Its pattern of harm is not “killing quickly,” but “debilitating large numbers of animals.” More concerningly, PoRV is showing a year-round disease trend, and its winter-spring seasonal pattern is no longer evident in some regions. This means it is no longer a problem that “needs to be controlled only in winter.”
PoRV control has an additional complication: the serotypes circulating in domestic pig populations are diverse, with G9, G5, G4, and G3 as the main types. However, commercially available trivalent live vaccines do not provide sufficient coverage, and cross-protection between different serotypes is limited. For PoRV, “a vaccine is available” and “the vaccine protects against the serotypes currently circulating” are two separate questions that need to be answered.
III. Mixed infections: PEDV+PoRV has become the dominant combination, systematically exacerbating disease
The variable most easily underestimated at present is how common mixed infections are and their clinical consequences.
The monitoring data from 2025 clearly show that among mixed infections involving multiple pathogens, PEDV+PoRV had the highest positivity rate, reaching 46.88%, far exceeding the 22.22% for PEDV+PDCoV. Another testing report based on more than one hundred pig farms likewise confirmed that mixed PEDV and PoRV infections accounted for 35.9% of diarrhea cases, while TGEV had almost disappeared from the range of mixed-infection combinations. The classic PEDV-TGEV combination is being replaced by PEDV-PoRV. This means that using traditional trivalent vaccines containing a TGEV component to address the current mixed-infection landscape leaves a structural gap in coverage.
The significance of mixed infection is not that there is “one more pathogen,” but that pathogenicity is amplified synergistically. PoRV infection can promote PEDV replication, and the two show a clear synergistic pathogenic effect in the intestine. Mixed infection causes a significantly higher mortality rate in newborn piglets than single infection. Meanwhile, although the overall detection rate of PDCoV is relatively low (most studies report less than 10%, though it can reach 48.10% in some submitted samples), it is endemic and can also exacerbate intestinal damage and immune dysregulation in newborn piglets when co-infecting with PEDV. In a sample already affected by mixed infection, designing an immunization and medication plan against only one of the pathogens effectively allows the other pathogen to continue causing losses.
Four. The limits of “feedback feeding”: an emergency tool, not a routine approach
Against a backdrop of inadequate protection from classic vaccines, feedback feeding has been taken up again by many pig farms. Feedback immunization with the G2c strain does indeed show, in the data, neutralizing antibody levels far above those of conventional vaccines—the GMT induced by the feedback strategy reaches 480—1893, 12 to 189.3 times the GMT of conventional vaccines (10—40). This data is genuine, but it describes the immunological potential under emergency conditions, not a routine procedure that can be standardized and widely promoted.
The core risk of feedback is not whether it “works,” but that the prerequisites for doing it correctly are extremely stringent. Without guidance from professional technical personnel, it is almost impossible to standardize and control the load of live virus in the infected material, the dose ratio for the sows receiving the feedback, and the overall pathogen background of the herd. More importantly, research in recent years has revealed the pathological mechanism by which live virus spreads through the “gut–mammary gland axis”: after a sow orally ingests live virus, the virus can be carried to the mammary gland by CD3+ T lymphocytes and enter the piglets’ intestines through the milk. The view that “live virus cannot immunize sows” is shifting from an academic judgment to a clinical risk that must be taken seriously. If the herd also carries pathogens such as PRRS, classical swine fever, or pseudorabies, indiscriminate feedback is tantamount to spreading the virus throughout the farm. It is reasonable to understand feedback as a “last resort”; using it as a “routine procedure” carries risks far greater than its benefits.
Five. A shift in prevention and control logic: from “relying on vaccines” to “managing transmission chains”
The current epidemiological situation points to an uncomfortable but necessary conclusion: under the combined constraints of immune escape by G2c and PoRV serotype diversity, existing commercial vaccines alone can no longer reliably reduce the clinical losses caused by viral diarrhea to an acceptable level.
The focus of prevention and control needs to be substantially shifted forward in three directions.
First, the quality of gilt acclimation is more critical than the number of additional vaccinations given to multiparous sows. A recurring finding in monitoring is that PED-IgA antibody positivity rates are low and highly variable at some pig farms, and are even negative. This directly reflects insufficient acclimation of replacement gilts before they enter the herd. In a sow herd with uneven immune backgrounds, the consistency of colostrum antibodies is difficult to ensure, no matter how many vaccinations are given before farrowing. Ensuring that gilts are exposed to locally circulating strains or receive targeted immunization before breeding, so their antibody levels are uniform when they enter the herd, is the first line of defense against the farrowing-room transmission chain.
Second, monitoring should shift from “testing after disease onset” to “parallel antibody and pathogen testing.” Both the G2c strain of PEDV and PoRV can continue shedding before or after clinical symptoms appear. A single negative pathogen test cannot rule out infection, and a single positive antibody test cannot distinguish between vaccination and a wild-type strain. Regularly monitoring PED-IgA antibody levels in the sow herd and the pathogen-carrier status of PoRV, combined with genomic sequencing to track changes in the strain type on the farm, reflects actual immunity gaps better than “vaccinating once when winter comes.”
Third, the importance of biosecurity in managing viral diarrhea needs to be raised again. Both PEDV and PoRV are transmitted mainly via the fecal–oral route. The roles of transport vehicles, feed logistics, personnel’s footwear, and tools in the transmission chain are far more significant than many pig farms are willing to admit. Standard cleaning and disinfection procedures cannot reliably remove PEDV from transport vehicles. This means that one-way movement at the loading area, transferring vehicles outside the farm, and all-in/all-out production with empty, dry farrowing rooms are not optional extras that simply make things “better”; after vaccine protection is reduced, they are the actual bottom line that determines whether the virus can enter the farrowing room.
Summary
The current prevalence of viral diarrhea in pigs can be summarized in three sentences: The G2c subtype of PEDV has become absolutely dominant, and there is a clear gap between the neutralizing antibody levels induced by classical vaccines and the pathogenicity of the virus; rotavirus has surpassed PEDV in detection rate, becoming the leading diarrheal pathogen by number; and PEDV+PoRV coinfection has replaced the classic combination as the most prevalent form of coinfection in current diarrhea cases.
The control strategy must change accordingly: instead of treating “vaccinating with the classical vaccine” as the default answer, greater priority should be given to the uniformity of gilt acclimation, regular parallel monitoring of antibodies and pathogens, and biosecurity in transport vehicle and farrowing-room procedures, rather than to “additional vaccination.” Feedback feeding may remain a technical option in emergencies, but it requires professional judgment and strict boundaries and cannot replace systematic management of transmission chains. The virus has already outpaced the vaccine; the precision of control must catch up. (Source: Zhang Weiguang)