With the application of novel, more sensitive and highly selective molecular biological techniques to porcine pathogen detection, epidemiological research on viral diseases that inflict substantial economic losses on the pig industry has been further advanced, accompanied by accumulating detection data of both emerging viruses and classical viral pathogens. Porcine parvovirus (PPV) is a major infectious agent triggering reproductive failure in swine. Until recently, PPV was thought to possess low genetic variability, and vaccination was considered effective in preventing PPV-induced reproductive disorders. Nevertheless, continuous research on this virus has raised doubts regarding the efficacy of current vaccines against emerging PPV strains. Subsequent studies have fundamentally reshaped our understanding of PPV evolution and immunology, as existing vaccines exhibit poor neutralizing capacity against newly emerged strains. These discoveries have greatly advanced our knowledge of PPV infection processes. This paper reviews the epidemiology, clinical manifestations and pathogenesis of porcine parvovirus disease, aiming to provide references for the prevention and control of PPV-caused reproductive disorders in sows.
Parvoviruses are a group of relatively small viruses with single-stranded DNA genomes ranging from 4 to 6.3 kilobases (kb). Ubiquitous in nature, parvoviruses are common infectious pathogens infecting a wide range of invertebrates and vertebrates. The ancestral parvoviruses are believed to have circulated globally millions of years ago. Despite descending from a common ancestor and sharing analogous genomic structures, parvoviruses generally display extremely low homology at the nucleotide or protein level, resulting in extensive genetic diversity. Such diversity dictates their clinical impacts on hosts, with infections ranging from asymptomatic non-pathogenic carriage to severe fatal diseases.
1 Prevalence of PPV1
In the early 1960s, reproductive failure prevailed in commercial pig farms and was largely attributed to nutritional and environmental factors. PPV was first isolated in Germany and later confirmed to be correlated with impaired reproductive performance in swine via experimental trials. Follow-up experiments verified that PPV-induced reproductive diseases manifest as sow infertility, mummified fetuses, stillbirths and abortions. PPV replicates primarily in fetal cardiomyocytes, leading to fetal death following transplacental infection during gestation. Previous epidemiological surveys on major etiologies of porcine reproductive failure identified PPV as a predominant cause of fetal mortality. A study conducted in the United States detected PPV1 in approximately 35% of stillborn piglets. A research project in Heilongjiang Province, China, confirmed PPV1 as the primary pathogen responsible for outbreaks of acute sow abortion. A Thai survey found PPV1 antibodies in 86% of sows suffering reproductive disorders. Owing to its exceptional environmental stability and capacity to infect pigs of all age groups and breeds, PPV1 is endemic across numerous regions worldwide.
1.1 Prevalence of Other PPV Genotypes
Since the initial identification of PPV1 in Germany roughly half a century ago, the adoption of molecular biological tools for pathogen discovery and detection has facilitated the identification of multiple novel PPV genotypes. The PPV2 genome was first accidentally detected in Myanmar swine, followed by reports of PPV2 circulation in Hungary, the United States, Japan, Germany, Thailand and other countries, with prevalence rates varying from 6% to 83%. PPV2 demonstrates high detection rates in tonsil samples, yet its tissue tropism and transmission routes remain unelucidated. PPV3 exhibits a global distribution, with documented cases in Asia, North America, Europe and Africa; wild boars in Germany and Romania tested positive for PPV3 at prevalence rates of 33% and 50%, respectively. PPV4 was initially discovered in North Carolina within PCV2-infected lung tissues, and subsequent positive detections have been reported in China, Hungary, Germany and Thailand at rates ranging from 2% to 44%. Phylogenetic analysis reveals that PPV4 shares closer evolutionary relatedness with bovine parvovirus 2 (BPV2). In recent years, several additional novel PPV species have been identified and tentatively designated PPV5, PPV6 and PPV7. A 2013 study characterized a new parvovirus sharing 64.1%–67.3% genomic homology with PPV4; phylogenetic reconstruction placed this virus on an independent evolutionary clade, which was provisionally named PPV5 with a 6.6% prevalence rate among U.S. swine. PPV6 was first isolated from aborted porcine fetuses in 2014 and later identified in serum samples collected from the United States and Mexico. Most recently, metagenomic sequencing of pooled samples uncovered a novel PPV strain in U.S. swine, which was subsequently detected in Chinese porcine serum samples and temporarily classified as PPV7.
2 Epidemiology of PPV
PPV1 is the earliest characterized porcine parvovirus, which circulates extensively in swine populations, infecting both domestic pigs and wild boars. Susceptible hosts include adult boars and sows, suckling piglets and finishing pigs. PPV1 infection has been identified in swine of all health statuses, including vaccinated and unvaccinated individuals, clinically healthy animals and diseased pigs. PPV’s remarkable environmental stability greatly enhances its infectivity and transmissibility. The virus can survive temperatures up to 90 °C, indicating outstanding thermostability. It also demonstrates partial resistance to common disinfectants such as ethanol and hypochlorous acid. PPV retains infectivity for months in contaminated pens, farming equipment and staff clothing, facilitating cross-farm transmission. Strict biosecurity protocols are mandatory for PPV prevention to block inter-farm viral spread. Imported PPV-contaminated semen can introduce the virus into naive pig herds. During natural mating, seronegative boars may contract PPV from infected sows. Additionally, PPV spreads horizontally within herds via feces, nasal secretions and oral exudates of infected pigs.
3 Clinical Manifestations of PPV Infection
The predominant clinical presentation of PPV infection is reproductive disease in gestating sows. When seronegative pregnant sows are infected in early gestation, conception is generally unaffected. However, embryonic PPV infection via transplacental transmission commonly causes embryonic death and resorption. Infections occurring after 35 days of gestation lead to fetal death and mummification. If infection takes place beyond day 70 of gestation, fetuses develop rudimentary immune competence, enabling them to resist PPV invasion and be delivered alive with positive PPV serology, presenting subclinical infection. Although PPV has been associated with secondary conditions including non-suppurative myocarditis, diarrhea, interstitial nephritis and cutaneous lesions in swine, its pathogenic role in these syndromes remains incompletely defined. Furthermore, PPV acts as a co-infectious pathogen that exacerbates the onset of post-weaning multisystemic wasting syndrome (PMWS) induced by PCV2.
4 Pathogenesis of PPV
In most cases, single PPV infection fails to trigger overt clinical signs in non-pregnant adult swine or piglets. PPV strain virulence is quantified based on the severity of resultant reproductive failure. The outcome of fetal PPV infection varies dramatically according to gestational age at exposure. Experimental and epidemiological evidence confirms that early-gestation PPV infection induces severe reproductive disorders, while fetuses infected after day 70 of pregnancy are usually delivered normally. Beyond gestational timing, viral genetic makeup is a decisive factor governing fetal infection outcomes. Low-virulence PPV strains and vaccine strains cannot penetrate the placental barrier, whereas highly virulent field strains possess this capability; direct injection of vaccine strains into amniotic fluid can still cause fetal death. The exact pathogenic cascade underlying PPV-mediated reproductive failure remains unclear, with the core unresolved question being how the virus crosses the placenta. To date, no evidence confirms PPV replication in uterine epithelial cells or trophectoderm, nor is there direct proof of macrophage-mediated viral trafficking from dam to fetus. Studies have verified that high-virulence PPV strains exhibit differential tissue tropism, which may account for variable initial embryonic infection capacity and divergent fetal clinical outcomes.
5 Prevention and Control Strategies
5.1 Strict Control of Infection Sources
For effective disease prevention and control, suspected cases must be immediately isolated and treated with appropriate medications, accompanied by comprehensive disinfection of pig housing. Severely diseased pigs with poor therapeutic response should be culled to thoroughly eliminate infection sources. All potentially exposed swine shall undergo serological testing via PPV ELISA kits to prevent viral dissemination from subclinically infected carriers. Pig farms should adhere to closed-pen breeding to minimize the risk of exogenous pathogen introduction. If herd expansion requires external pig introduction, thorough regional epidemiological investigations must be conducted, and procurement from epidemic areas is prohibited. Newly introduced pigs shall be quarantined for 1 to 2 months and mixed with resident herds only after testing negative for PPV.
5.2 Regular Disinfection Protocols
Farm staff must establish standardized disinfection awareness and implement proper disinfection procedures. Pen manure shall be cleared daily to maintain dry flooring and establish a hygienic rearing environment. Strict access control for personnel and vehicles is enforced with mandatory disinfection measures: 2% sodium hydroxide solution for vehicle sterilization, 75% ethanol for incoming and outgoing staff, formalin spray for pen floors and wall corners, and formalin topical disinfection for swine bodies to optimize disinfection efficacy.
5.3 Preventive Vaccination
Vaccination constitutes an effective preventive measure against PPV. In breeding pig farms, inactivated vaccines are widely applied, categorized as tissue-origin inactivated vaccines and cell-cultured inactivated vaccines. Vaccination schedules are specified as follows: gilts receive oil-adjuvanted cell-cultured inactivated PPV vaccines at approximately 20 weeks of age; replacement breeding females are immunized with PPV inactivated vaccines three weeks prior to mating; multiparous sows are vaccinated two weeks post-farrowing; breeding boars receive two annual immunizations (spring and autumn) to sustain protective antibody titers in the herd. Post-vaccination serological monitoring shall be performed regularly, with timely supplementary immunization administered for missed vaccinations.
Conclusion
In recent years, rapid progress has been achieved in PPV detection technology, diagnostic reagent development and vaccine research, alongside extensive global epidemiological investigations into PPV and novel PPV genotypes. Nevertheless, numerous critical gaps persist regarding PPV biology, pathogenic mechanisms and novel strain detection methods, most notably the molecular pathway enabling PPV to traverse the placental barrier and infect fetuses. Additionally, emerging novel PPV strains pose substantial challenges to the protective efficacy of conventional vaccines. Several newly identified PPV variants display close genetic relatedness to human parvoviruses, which necessitates large-scale surveillance to screen for strains with potential zoonotic risks. Comprehensive identification of PPV and other easily neglected swine pathogens is essential for herd health management. Meanwhile, novel PPV genotypes compromise the reliability of existing routine PPV detection assays. Therefore, future research shall prioritize elucidating PPV pathogenic mechanisms, conducting systematic epidemiological surveys, developing innovative diagnostic reagents and vaccines, and formulating scientific, targeted PPV control programs to mitigate economic losses caused by porcine parvovirus infection in pig production systems.
Translation Notes
Professional veterinary terminology complies with international standard nomenclature for swine diseases:
木乃伊胎：mummified fetuses；断奶仔猪多系统消耗性综合征：post-weaning multisystemic wasting syndrome (PMWS)
油佐剂灭活苗：oil-adjuvanted inactivated vaccine；组织灭活苗：tissue-origin inactivated vaccine
Genotype abbreviations unified: PPV1–PPV7, PCV2 (Porcine Circovirus Type 2), BPV2 (Bovine Parvovirus 2)
Numerical units, gestational days, disinfectant concentrations and quarantine cycles retained original values consistent with veterinary academic writing conventions
Long Chinese complex sentences restructured into logical English compound sentences without altering original research meaning; academic tone maintained for veterinary journal submission suitability