Porcine endogenous retroviruses (PERVs) are gamma retroviruses integrated in the genome of all pigs. There are three different PERV subtypes: PERV-A, PERV-B and PERV-C [
1]. Whereas PERV-A and PERV-B are integrated in the genome of all pigs, PERV-C is found in many, but not all pigs. PERV-A and PERV-B infect cells from numerous species including human cells [
1‐
3]. The human porcine endogenous retrovirus-A receptor 1 and 2 (huPAR1 and huPAR2, respectively) are receptors for PERV-A [
4]. They are members of the riboflavin transporter, also known as human riboflavin transporter 3 (hRFT3), and human riboflavin transporter 1 (hRFT1), respectively. More recently, these receptors have been renamed and classified as members of the solute carrier family of receptors, “solute carrier family 52A” (SLC52A) [
5]. huPAR1 and huPAR2 are present on human cells, related receptors are present on other species, determining the host range. The PERV receptor on baboon and other non-human primate cells is functional, but deficient by a mutation, explaining the low replication in these cells [
6]. Mice have a mutated receptor, explaining that mouse cells could not be infected, and rats have only a low expression of a functional receptor, explaining that rat cells could not be infected [
7]. However, transfection with human or rat PAR-1 conferred susceptibility [
7]. The receptors for PERV-B and PERV-C are still unknown. PERV-C is in contrast to PERV-A and PERV-B an ecotropic virus, infecting only pig cells [
8]. The envelope proteins of the viruses are responsible for infection. The receptor-binding domain of the surface envelope protein interacts with the cellular receptor and the transmembrane envelope protein is responsible for the fusion between viral and cellular membranes [
1]. In some pigs recombinants between PERV-A and PERV-C were found [
9]. The recombinant viruses contain the receptor-binding domain of PERV-A and most of the PERV-C genome, including the PERV-C-specific long terminal repeats (LTRs). The recombination point in the envelope gene (
env) is well known, however the second recombination point, which should be upstream of the
env gene is not known. PERV-A/C viruses are replication competent in living pigs and numerous copies were found in different organs of these pigs, but never in the germ line. PERV-C-positive miniature pigs from the USA have been shown to harbour such PERV-A/C viruses [
9,
10] and their mitogen-stimulated PBMCs released human-tropic viruses able to infect 293 cells [
11]. PERV-A/Cs were also found in Yucatan micropigs and their PBMCs were characterised by a high expression of PERV and release of reverse transcriptase (RT) activity into the supernatant [
11‐
13]. Until now PERV-A/Cs were described with one exception only in minipigs, possibly as the result of inbreeding, higher numbers and higher expression of PERV-C in these animals (for review see [
9]). In a previous publication we analysed GöMPs produced at Ellegaard Göttingen Minipigs A/S (Dalmose, Denmark) and did not find any PERV-A/C in the PBMCs from five animals [
14]. Recently, we screened Göttingen minipigs produced at the University of Göttingen (Göttingen, Germany) for the presence of human-tropic PERVs and found that mitogen-stimulated PBMCs from one of 11 analyzed animals, named pig F, were able to infect human 293 cells, either by the release of cell-free virus or by cell-to-cell transmission [
15]. One of these mechanisms is a prerequisite for the infection of recipients after xenotransplantation. However, this is a rare event: In our experiment, PBMCs from one of 11 Göttingen minipigs from the University of Göttingen were able to infect human 293 cells, either directly or cell-free by released virus [
15]. Here, we give an extended analysis of this virus including changes in the long terminals repeats (LTRs) during passaging on human cells. In order to evaluate the probability of the virus release, the experiment was performed with other pigs, including new GöMPs.