Avian leukosis viruses (ALVs) have been virtually eradicated from commercial poultry. However, some niches remain as pockets from which this group of viruses may reemerge and induce economic losses. Such is the case of fancy, hobby, backyard chickens and indigenous or native breeds, which are not as strictly inspected as commercial poultry and which have been found to harbor ALVs. In addition, the genome of both poultry and of several gamebird species contain endogenous retroviral sequences. Circumstances that support keeping up surveillance include the detection of several ALV natural recombinants between exogenous and endogenous ALV-related sequences which, combined with the well-known ability of retroviruses to mutate, facilitate the emergence of escape mutants. The subgroup most prevalent nowadays, ALV-J, has emerged as a multi-recombinant which uses a different receptor from the previously known subgroups, greatly increasing its cell tropism and pathogenicity and making it more transmissible. In this review we describe the ALVs, their different subgroups and which receptor they use to infect the cell, their routes of transmission and their presence in different bird collectivities, and the immune response against them. We analyze the different systems to control them, from vaccination to the progress made editing the bird genome to generate mutated ALV receptors or selecting certain haplotypes.

There is growing interest in emerging viruses that can cause serious or lethal disease in humans and animals. The proliferation of cloacal virome studies, mainly focused on poultry and other domestic birds, reveals a wide variety of viruses, although their pathogenic significance is currently uncertain. Analysis of viruses detected in wild birds is complex and often biased towards waterfowl because of the obvious interest in avian influenza or other zoonotic viruses. Less is known about the viruses present in the order Passeriformes, which comprises approximately 60% of extant bird species. This review aims to compile the most significant contributions on the DNA/RNA viruses affecting passerines, from traditional and metagenomic studies. It highlights that most passerine species have never been sampled. Especially the RNA viruses from Flaviviridae, Orthomyxoviridae and Togaviridae are considered emerging because of increased incidence or avian mortality/morbidity, spread to new geographical areas or hosts and their zoonotic risk. Arguably poxvirus, and perhaps other virus groups, could also be considered “emerging viruses”. However, many of these viruses have only recently been described in passerines using metagenomics and their role in the ecosystem is unknown. Finally, it is noteworthy that only one third of the viruses affecting passerines have been officially recognized.

Using fluorescent protein-tagged F-actin reporters we studied the actin cytoskeleton in Aspergillus nidulans. F-actin probes labeled endocytic patches, contractile actin rings and the Spitzenkörper (SPK), but not exocytic cables generated by the SPK-associated formin, illuminated only by tropomyosin. The SPK actin mesh contains tropomyosin and capping protein, but not fimbrin or Arp2/3, showing that it does not involve branched actin. Arp2/3 and fimbrin are recruited to endocytic patches at the end of their lifecycle, staying in them for 12–14 sec, coinciding with the burst of branched actin polymerization that powers vesicle internalization, whereas verprolin stays only during the first half of this actin phase. Hyphal growth requires endocytic recycling, which we exploited to assess the efficiency of endocytosis following genetic interventions. Ablation of SlaB^Sla2, Arp2/3, cofilin and fimbrin is lethal, whereas that of Srv2, verprolin and capping protein are debilitating, with the lifetime of actin in mutant patches roughly correlating with the extent of growth and endocytic defects. An outstanding problem is the origin of seed filaments required to prime Arp2/3 during endocytosis. Actin patches associate with cortical cables that give rise to long distance-moving “actin worms” that are different from tropomyosin-containing cables emanating from the SPK. Cables and worms are dependent on formin, yet inactivation of formin does not affect the F-actin patch lifecycle, arguing against formin playing an endocytic role. Ablation of the WISH/DIP/SPIN90 protein Dip1 priming Arp2/3 for the synthesis of linear actin delocalizes the endocytic machinery and severely impairs, but does not preclude, endocytosis. This establishes the existence of Dip1-independent mechanism(s) that synthesize seed filaments. Our data negate the possibility that this alternative mechanism results from a priming role of formin that is unmasked in dip1∆ cells, but do not exclude that cofilin-mediated filament severing could produce seed microfilaments for Arp2/3, as suggested for Schizosaccharomyces pombe.

One of the main threats for the survival of the Iberian lynx is infectious disease. Feline parvoviruses cause often fatal diseases in cats and have been isolated from different species of Felidae and other carnivores. The present study is the first description of a parvoviral sequence isolated from the brain of an Iberian lynx which died four weeks after being transferred to a quarantine centre from a hunting estate in Castilla-La-Mancha (southern border of the Iberian plateau). Four days prior to death, it had developed anorexia and muscle weakness. The nucleotide sequence, at 4589 nt long (GenBank PP781551), was most proximal to that isolated from a Eurasian badger in Italy but also showed great homology with others from cats and other carnivores isolated in Spain and Italy, including that from a cat sequenced by us to elucidate the origin of the infection, which has not been clarified. The phylogenetic analysis of the capsid protein, VP2, which determines tropism and host range, confirmed that the lynx sequence was most proximal to feline than to canine parvoviruses, and was thus typed as Protoparvovirus carnivoran1. More studies, including serology, are needed to understand the pathogenesis of this infection.

The Genus Alpharetrovirus contains viruses pathogenic mainly for chickens, forming the Avian Sarcoma and Leukosis Virus group (ASLV). Cells of most Galliform species, besides chickens, contain genetic elements (endogenous retroviruses, ERVs) that could recombine with other alpharetroviruses or express proteins, complementing defective ASLV, which may successfully replicate and cause disease. However, they are quite unknown, and only ALV-F, from ring-necked pheasants, has been partially published. Upon scrutiny of 53 genomes of different avian species, we found Alpharetrovirus-like sequences only in 12 different Galliformes, including six full-length (7.4–7.6 Kbp) and 27 partial sequences. Phylogenetic studies of the regions studied (LTR, gag, pol, and env) consistently resulted in five almost identical clades containing the same ERVs: Clade I (presently known ASLVs); Clade II (Callipepla spp. ERVs); Clade IIIa (Phasianus colchicus ERVs); Clade IIIb (Alectoris spp. ERVs); and Clade IV (Centrocercus spp. ERVs). The low pol identity scores suggested that each of these Clades may be considered a different species. ORF analysis revealed that putatively encoded proteins would be very similar in length and domains to those of other alpharetroviruses and thus potentially functional. This will undoubtedly contribute to better understanding the biology of defective viruses, especially in wild Galliformes, their evolution, and the danger they may represent for other wild species and the poultry industry.

One of the main threats for the survival of the Iberian lynx are infectious diseases. Feline parvo-viruses cause an often fatal disease in cats and have been isolated from different species of Felidae and other carnivores. The present study is the first description of a parvoviral sequence isolated from the brain of an Iberian lynx which had died four weeks after been transferred to a quarantine centre from a hunting estate in Castilla-La-Mancha (southern border of the Iberian plateau). Four days prior to death he had developed anorexia and muscle weakness. The nucleotide sequence, 4,589 nt long (GenBank PP781551), was most proximal to that isolated from a Eurasian badger in Italy but showed also great homology with others from cats and other carnivores isolated in Spain and Italy, including that from a cat sequenced by us to elucidate the origin of the infection, which has not been clarified. The phylogenetic analysis of the capsid protein, VP2, which determines tropism and host range, confirmed that the lynx sequence was most proximal to feline than to canine parvoviruses, and was thus classified as Protoparvovirus carnivoran 1. More studies, in-cluding serology, are needed to understand the pathogenesis of this infection.