Is PRRSV 1C.5 more airborne than other variants?

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The rapid spread of porcine reproductive and respiratory syndrome virus variant 1C.5 (aka L1C 1-4-4) a few years ago prompted the question whether this newly identified PRRSV variant was more transmissible through the air than other endemic variants circulating at that time in pigs.

The Torremorell research lab, in collaboration with faculty in the Swine Group at the University of Minnesota College of Veterinary Medicine and faculty in Mechanical Engineering sought to answer the question whether aerosolization of clinically relevant PRRS virus differs among variants and if so, are the differences due to the particle size, load and viability of virus-laden aerosols, and whether infected pigs with different clinical affectation differ in their ability to generate airborne viruses. To address this question, we systematically evaluated the stability of variants in experimentally generated aerosols and also compared levels and trends of virus-laden particles in aerosols collected from experimentally infected pigs.

The stability of PRRSV in aerosols was evaluated for six clinically relevant PRRSV variants recovered over the years (VR2332 (L5), MN30100 (L9A), L1C.5 1-4-4, L1A 1-7-4, L1F 1-8-4, and Lelystad virus). Using state of the art methods consisting of a 40 L Biaera Goldberg rotating drum, aerosols were injected into the drum, rotated for up to 120 minutes and air samples collected at various time points to evaluate total viral RNA and viable PRRSV.

Overall, we observed differences in the decay patterns of the various viral variants. Differences were more notable for viral viability, where the decay of viable virus was faster than that of RNA. Among all variants tested, MN-30100 (L9A) preserved its viability at all time points with higher viral load (1.75-2.5 logs) and detection in broader particle size ranges of <4.7 μm. In contrast, viability of reference variant VR-2332 was only documented at 30 and 60 min at levels of 1.75 and 2 logs and the viability of variant L1C.5 1-4-4 was only detected at time zero, and at 120 min for 1 sample, with a viral load of 1.75 logs. For the other variants, viability was limited to very few samples at 1.75 logs or non-detectable, likely in part due to lower initial virus concentrations and sensitivity of the viral titration methods. These results did not support the general assumption that variants considered of high virulence had higher stability or viability in aerosols.

To further investigate differences between variants and implications for PRRSV transmission in the field, a model using experimentally infected pigs was used. Pigs at weaning were inoculated with one of three distinct variants (L1C.5 1-4-4, L1A 1-7-4, and MN-30100 (L9A)), and one group was left unchallenged. The first two isolates were selected due to their high prevalence and clinical relevance in recent years, while the L9A isolate was included based on prior studies demonstrating airborne transmission and lower virulence. After challenging, pigs were observed clinically, bled and nasal swabs collected at various time points after infection and throughout the study. Air samples were also collected using a battery of air samplers to maximize detection of virus in the air.

There were differences among the three variants in terms of clinical impact. Pigs in groups L1C.5 1-4-4 and L1A 1-7-4 were the most affected, showing severe respiratory signs, lethargy, reduced feed intake, higher body temperatures (fever), and lower body weights and growth rates. In terms of viremia, all inoculated pigs became infected, with variant L1A 1-7-4 showing a higher and more sustained viral load, followed by variant L1C.5 1-4-4 which also resulted in a significant viral load, in particular within the first seven days post infection. Viral load for both of these variants decreased after 15 days post infection. Interestingly, variant MN30100 had the lowest viral load during the first seven days of infection, but viral load remained relatively elevated throughout the rest of the study. Similar trends were observed for nasal shedding, with the difference that shedding of L1C.5 1-4-4 was lower after 11 days post infection compared to the other two variants.

In terms of PRRSV detection in the air, all three variants were detected consistently in the air, although detection patterns differed slightly. Detection was most similar during the first 10 days post infection, with variant L1A 1-7-4 having the highest and most sustained levels of virus in the air. Interestingly, L1C.5 1-4-4 variant after 13 days post-infection became non-detectable in the air. Lastly, in terms of particle size distribution, for most days of the study, all variants could be detected in particles above 9 μm, and detection in particles between 9.0 and 4.7 μm was less consistent. 

Overall, these results suggest that there are differences among PRRSV variants in terms of their ability to become airborne. Although the full analysis of all the results is still in process, the data so far indicate that differences may be explained in part by differences in pathogenicity and nasal excretion levels. If results from this study are taken together with a recent publication by Melini et al., (2025) that indicates that the infectious dose of PRRSV L1C.5 1-4-4 is very low, it doesn’t take a lot of virus to facilitate transmission and cause disease.

Ultimately, the key question is whether we need to develop or adjust biosecurity procedures that are dose-dependent (e.g. air filtration) to be effective. Results from this study should instigate the development of more effective strategies to prevent the introduction of new variants into farms, including variants with a higher propensity to transmit through the air.

This article was written by Montse Torremorell and Juan Mena of the University of Minnesota for the National Hog Farmer

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