Porcine reproductive and respiratory syndrome virus (PRRSV) has caused significant economic losses in the swine industry worldwide [1] [2] . Losses range from 75 thousand euros in a farm with a thousand sows with a “light” infection, to losses of 698 thousand euros [2] and 664 million dollars per year in the USA [2] ) or 1.8 million dollars per day [3] .

PRRSV causes significant economic losses to the farm, regardless of the pathogenicity of the strain, since a primary infection can cause losses from an outbreak and to this are added the losses due to the permanence of the disease in endemic form, with the possibility of re-emerging as an outbreak. acute after a long period of the last outbreak and are outbreaks that take 2 to 3 months to subside. Losses on the farm due to the endemic form are slight, but constant due to a decrease in fertility rates and weight gain, and increases costs by associating it with other respiratory diseases [4] .

It is important to remember that PRRSV leaves serious economic losses on large or small farms, both in abortions and neonatal mortality, as well as in growing and fattening areas, and mostly causes many fertility problems that delay production. PRRSV is an RNA virus that exploits all known mechanisms of genetic variation to ensure its survival. Distinctive features of RNA virus replication include high mutation rates, high yields, and short replication times. As a consequence, RNA viruses replicate as complex and dynamic mutant swarms, called viral quasispecies, such that they are a major problem for swine production.

According to Meulenberg et al. [5] the causal agent is an RNA virus called PRRSV. This virus belongs to the order Nidovirus, family Arteriviridae and genus Arterivirus, [6] [7] [8] . The PRRS virus particle has a diameter between 50 and 65 nm, with a central isometric nucleocapsid approximately 30 to 35 nm in diameter [7] . The genome of the PRRS virus is 15 kb positive-strand RNA, containing seven open reading frames (ORFs).

PRRSV, being a small enveloped virus, has a positive-sense stranded RNA genome [4] [9] , and is ~15 kb in length [3] [4] . It contains 11 open reading frames (ORFs), including ORF1a, ORF1b, ORF2a, ORF2b, ORF3, ORF4, ORF5a, ORF5, ORF6, ORF7, and a short trans frame (TF) ORF. transframe) in the non-structural proteins 2 (nsp2) region. These ORFs encode 16 non-structural proteins (nsp1α, nsp1β, nsp2-nsp6, nsp7α, nsp7β, nsp8-nsp12, nsp2TF and nsp2N) and eight structural proteins (SP), which are: GP2, E, GP3-GP5, GP5a, M, and N [3] .

The ORF 1a and 1b genes, located at the 5 end, occupy 80% of the genome and encode the replicase and proteins involved in the replication and transcription of the viral RNA. ORFs 2-5 encode GP2, GP3, GP4 and GP5, and ORF6 and ORF7 encode the M protein and the nucleocapsid (N), respectively [10] .

In stallions, clinical manifestations include anorexia, lethargy and low libido [11] [12] , consequently, there are alterations in semen quality, including a decrease in sperm motility, an increase in morphoanomalies. and increase in sperm with distal cytoplasmic droplets between days 35 and 42 post-infection [13] , alterations in semen quality are directly correlated with fertility parameters [14] .

The virus has been found in the seminiferous tubules, reaching the germ cells by migration of macrophages to the interstitial cells of the testis and by hematogenous dissemination [15] . Another route of PRRSV transmission is artificial insemination when semen from infected insemination centers is handled. Due to the above, the study is focused on evaluating the effect of PRRSV on the motility of Boar sperm, when infected with viral particles, because motility is an essential property of the cell and its alterations have been associated with problems of fertility [16] and [17] . Individuals with low sperm motility are considered infertile [17] .

The work was carried out in the Genetics and Reproduction laboratory of Facultad de Medicina Veterinaria and Zootecnia from the Benemérita Universidad Autónoma de Puebla.

The semen was evaluated every 24 hours for ten days, taking as reference the Total Cells Observed, Virus Concentration and Days Post Infection. (P ≤ 0.05) were observed regarding the number of cells with Total Mobility on the different evaluation days. 201 ± 7.3, 167 ± 10.1, 165 ± 14.6, 134 ± 8.2 and 120 ± 8.8 for days 1, 3, 5, 7 and 10, respectively.

At the same time, there was no (P ≥ 0.05) between the control and virus concentrations with respect to the Progressive Mobility percentages.

Table 3 shows that the concentration of sperm cells decreases as the days post-infection increase.

In Table 4, it is observed that the Curvilinear Velocity on days 1 and 7 Post-Infection at the 10X² and 10X⁶ concentration exists a significant difference (P < 0.05) compared to the control group.

In Table 5. It is observed that the Rectilinear Speed on day 1 Post-Infection at the concentrations 10X², 10X⁴ and 10X⁶ is a significant difference (P < 0.05) compared to the control group.

Table 6. It is observed that the Linear Velocity on day 1 post-infection at the concentration 10X², 10X⁴ and 10X⁶ there is a significant difference P < 0.05 compared to the control group

Table 7. The amplitude of Lateral Displacement shows that on days 5 and 7 Post-Infection at the concentration 10X⁴ and 10X⁶ there is a significant difference P < 0.05 compared to the control group.