LOS RETROVIRUS: UNA REVISION Biochonologically
Raúl H. Rosadio A. 
is now possible to understand and explain the mechanism of many chronic consumptive character, until the discovery of unexplained behavior of a set pathobiologically viral, now known as retroviruses or lentiviruses. Raul Rosadio, very swiftly reviewed and discussed the biochronology of retroviruses of veterinary interest and the similarities with the AIDS virus. In the eighties, the emergence of the pandemic known as acquired immunodeficiency syndrome (AIDS) in humans triggered retrovirology fashion and an unusual interest in the association of infections retroviral and chronic diseases. The isolation of the causative agent of AIDS retrovirus, aroused a great hope to find early solution to the illness of the century through the use of candidate vaccines. Was not long before the scientific community in understanding the biology of human immunodeficiency virus (HIV) was more complicated than imagined, and that the long-awaited vaccine would have to wait to have better understanding of retroviral biology. These frustrations are to be redeemed and knowledge studies described retroviral infections in veterinary medicine. Also, encourage new clinical studies and / or experimental in order to understand the pathobiology of infections similar observed in many species of animals.
This analysis, describing historically retroviral infections in animals, try to point out the great contribution that these studies have achieved for basic information and knowledge of the etiology and mechanisms of retrovirus infection in chronic conditions.
The association between retroviruses and chronic diseases in various species of animals is not recent history. A large majority of these infections, described since the beginning of the century, are producers of chronic clinical course variables. Infected animals, depending on the evolutionary process of infection, often do not show clinical disease, but a good number of these patients suffer from chronic proliferative processes, degeneration, immunodeficiency, and / or neoplastic processes.
The first suspicion of retroviruses to cause disease in animals, comes from 1910 with the demonstration of a filterable agent, now called the Rous sarcoma virus, produced tumors in muscles, bones and blood tissue aves.1 These findings were met with some skepticism and criticism eventually stop early studies of retrovirus as a possible cause of cancer. Then in the 1950s, Gross and other researchers Ludkit reported similar tumor-associated retrovirus in ratones.2 Despite this new evidence reinforced the hypothesis of Dr. Rous on the possible relationship between retroviruses and cancer, they were not quite enough to convince the scientific community. The fact that the retrovirus isolates came from animals bred and kept in the laboratory (high inbreeding) were sufficient grounds to keep the disbelief. Was based, moreover, that viral transmission in these animals was mainly congenital, via almost improbable to be observed in humans. Great skill was unknown Held retroviru s to be inserted into the cellular genome, and therefore potentially be
Perhaps oncogénicos.3
one of the earliest reports on the possible association of retroviruses and chronic illness and / or cancer in pets come from the late XIX.4 The domestic sheep when introduced to South Africa showed a greater susceptibility to infection associated chronic consumantes respiratorios4 mainly syndromes. In these descriptions, recorded in official correspondence of European immigrants, they use jaagsiekte disease "to describe African term fatigue and respiratory distress in animals subjected to large initial caminatas.5 knowledge of this and other chronic diseases in sheep consumantes yet are due in large part to researchers Icelanders.
In the 1930s, Iceland in an effort to improve their genetic potential shepherd rams imported a lot from Germany, and with them a group of epizootic disease and high fatality for native sheep population. Studies of these diseases clearly distinguish two types of clinical manifestations, respiratory form called Icelandic "Maedi" and other nervous reported as "Visna" .6 The Icelandic sheep also showed increased susceptibility to jaagsiekte described by South African farmers. 6 All these diseases have one thing in common, progressive course was chronic and usually fatal to a population apparently immunologically virgin or agents introduced to the import. The Icelandic researchers led by Dr. Sigurdson, in an attempt to seek explanations for the disease observed, hypothesized that these diseases were viral products slow and progressive action. Although the evidence showed the presence of viral agents capable of causing disease with extremely long incubation periods (months and even years), the scientific community took about half a century to accept the concept and the biology of virus infections losdenominados slow (lentivirus).
The concept of retrovirus and chronic infections and Cancer begins to change in 1960, thanks to the discovery of feline leukemia virus by brothers, William and Oswald Jarrett, veterinarians at the University of Glasgow. They showed that cats were susceptible to infection by retroviruses, and consequently suffering from leukemia, lymphoma, aplastic anemia and immunodeficiency syndrome very similar to what later became known as AIDS humanos.7 These same researchers also demonstrated retrovirus infections that were not laboratory curiosities, as home-reared cats were also susceptible to infection. These new contributions were not quite enough for the reluctant community accepted scientific relationship retroviral infections with several types of chronic diseases, mainly cancer. The argument of the day, was the fact that most reported retroviral infections were caused by retroviruses "exogenous" (similar to virus transmission capacity to insert common in genomes of somatic cells) and not by virus "endogenous" (like transmission Mendelian genes, able to integrate into the genome of germ cells in very low pathogenicity) commonly reported as able to induce spontaneous lymphomas and breast carcinomas in murino3 system.
pioneering studies carried out in Iceland, they encouraged researchers in many countries to search Shepherd emaciantes disease, progressive similar to those described in Iceland. Product of these concerns are described in various parts of the world, chronic penumonias (Maedi, chronic progressive pneumonia), jaagsiekte like diseases (pulmonary adenomatosis, ovine pulmonary carcinoma), progressive paralysis (Visna) .8,9,10,11 Then in the 1960s, the viral theory of some of these diseases was supported with viral isolates from clinically diseased animals and infected organs in the laboratory. The isolated virus takes its name from the disease syndrome described (Maedi virus, virus of Visna, etc.), but researchers only focus on testing the proposition Kosch.12 These reports, however, demonstrate the existence of certain oncogenic retrovirus without capacity, suggesting the creation of a new subfamily and Maedi viruses as subfamily prototype Lentivirinae.3
Later and thanks to the discovery of a specific enzyme of retroviruses, reverse transcriptase, and the enormous progress made in cell culture isolates of retroviruses of various species of domestic animals progresivamente.13 With increasing the help of these new biological tools, from the early 70s retrovirus isolates spread to other species pets. Thus, achieved the isolation of bovine leukemia retrovirus causing malignancy of blood cells and lymphatic organs (leukemia and lymphoma) in cattle, 14 the producer retrovirus equine infectious anemia, 15 and the retrovirus that causes encephalitis and arthritis in goats (goat lentivirus) .16
Similar studies performed in animal wildlife, retrovirus isolated from breast tumor lesions in old world monkeys (rhesus monkeys) .17 The possible association of breast cancer retrovirus in monkeys, created the enthusiasm of researchers in attempting to demonstrate that the isolate was a retrovirus similar to oncogenic virus producer breast cancer in mice (type B retrovirus) .18 To this end, young rhesus monkeys were inoculated with the retrovirus isolated. Surprisingly, the animals bred breast tumor lesions but inoculated monkeys had high susceptibility to severe and fatal infections, oral, respiratory and digestive related to micro-organisms will patogénicos.18 disappointed with the inability to replicate breast cancer lesions, the authors frozen strain show no interest in the paintings now known as immunodeficiency. Years later, because of the outbreak strain of simian AIDS thawed and restarts the associated retrovirus interest in box immunodeficiency in monkeys. Recent experimental studies have shown that retrovirus Mason-Pfizer-like (type D retrovirus) and lentivirus (simian immunodeficiency virus) are capable of producing immunodeficiency syndrome in macaque monkeys raised in cautiverio.19, 20
The discovery of lentivirus morphological features and physico-chemical characteristics similar to Maedi virus as causative agents of various diseases in different species of animals and even humans, awakened an unusual interest in understanding the mechanisms of disease and especially to elucidate the molecular pathobiology. Science uses the skills of biochemical, genetic and related to study and obtain information at the molecular level and especially biological properties of some gene products. These new efforts show that the genome has three genes necessary for replication and oncogenic capacity of Rous virus lies in a specific gene called src (sarcoma) .21, we show that the src gene is not exclusively as it is also viral present in normal cells of birds, apparently fulfilling the control functions celular.21 These findings suggest that during the genetic evolution, Rous virus has captured and taken over the cellular src gene, which under the control turns acquires tumorigenic characteristics (retrovirus oncogenic treble).
However, the viral genome the vast majority of oncogenic avian and murine retroviruses have not oncogenes.22 These viruses, known as acute non-oncogenic, cell transformation produced by mutagenic activation mechanism called insercional.22 proviral DNA integration into the genome potentially oncogenic cell can directly damage cellular genes or alter their gene expression to seize control using powerful cellular proviral regulatory elements such as LTR (long-chain repeats). The activation and promotion of certain genes occurs when the retroviral provirus is inserted adjacent to genes regulating development, division or differentiation. This mechanism of tumorigenesis is specific and generally active regulatory genes such as c-myc in the majority of leukemias and lymphomas observed in birds, mice and ratas.23 Other times, the retroviral insertion into two other gene critical for the excessive control of cell growth and inactivating (Cellular gene repression) 24.25 These findings allowed to identify cellular genes that may participate in tumorigenesis and opened all possibilities to solve the mystery of how normal cells control their growth and neoplastic fail in hacerlo.26, 27
Research with the leukemia virus bovine exogenous B-lymphotropic virus, have shown great affinity that retroviruses have high-powered cell-proliferative and especially for those immunologically privilegiadas.28, 29 The bovine leukemia virus produces several types of events such as persistent lymphocytosis, non-neoplastic proliferation of B cells, EBL, and neoplastic cell proliferation B.28, 29 The various clinical manifestations of viral infection in cattle suggests a multistep process, often with inapparent clinical course or progress toward ending persistent lymphocytosis with tumor formation in lymph nodes or other órganos.29 During persistent lymphocytosis associated with a polyclonal proliferation of infected B cells facilitate retroviral integration. Apparently the viral infection and gene expression are necessary to maintain the proliferative and tumor induction process, but unnecessary once turnorales cells have been established. Have not observed the presence of viral or cellular oncogenes in the process leucomogénesis. The viral genome has an extra gene that acts differently to an oncogene, has properties of transcriptional activation (tax gene) that increases transcription of the viral LTR and genes celulares.30 The mechanism of malignant transformation is not fully elucidated molecular level, but leucomogenesis speculated that during the presence of tax protein is necessary but not sufficient to maintain the progression tumorogénica.30
The feline leukemia virus is a cat's natural disease associated with various clinical manifestations such as anemia, proliferative processes, Immunosuppression and neoplasia. The various types of clinical lesions observed in the infected animal will depend on the viral genotype involved and the efficiency of the immune system of the infected animal Yes hospedero.31 produce enough antibodies neutralizing the infecting virus will be restricted and controlled at the level of cellular provirus . Not occur, the disease progresses from preleucémica phase to form pictures or proliferative inmunosupresión.31 The virus has three envelope antigenic types (A, B and C), subtype A in nature is always as simple genotype, while genotypes B and C usually associated observed with the A .32 The different cell tropism observed in this virus, perhaps due to the properties of glycoproteins and LTR sequences proviral.33 typical viral genome has no oncogene, but has a great ability to recombine with viral variants with a variety of cellular sequences. There is evidence that the types B and C are products of genetic recombination between subtype A and endogenous gene sequences very similar. 31 The combinations of types A + B syndrome are associated with immunosuppression and AIDS-like processes (feline AIDS) 33-34 leucomogenesis mechanism is not entirely well elucidated, but certain viral and cellular recombination would give rise to viruses capable of tumor There linfomas.31 and produce viral insertions adjacent information and / or presence of molecular disorder gene c-myc suggesting similar mechanism to that observed in neoplasms of birds and ratones35. However, defective viruses have been identified containing myc gene in lymphosarcoma of the thymus, suggesting the existence of recombinant viruses that have oncogenes.35
The association of retroviruses and carcinomas is much more uncertain but there are reports of its presence in more than one species of animal. The mice are highly susceptible to infection by type B retrovirus (retrovirus murine mammary carcinoma) which often end up producing mammary carcinomas in animals portadores.36 proviral DNA contains an extensive LTR containing an open reading frame (ORF) capable to produce a protein of 320 amino acids. 37 An interesting feature of the biology of murine B retrovirus, is the induction of T cell lymphomas in carrier. 36.38 vertically transmitted virus from mothers to infants primarily infected milk, but recent research also mention that the virus is transmitted Mendelian manner (endogenous) .37 This apparent duality, would result from a recent (evolutionarily) viral infection of germ cells in their desire to acquire resistance to exogenous infections. 37.39 The orf gene would help in early infection, to induce proliferation of lymphoid cells by promoting viral integration and use these cells to spread the virus, so that later and for a totally unknown mechanism to infect epithelial cells. 39 Surprisingly, the orf gene has biological activities similar to known superantigen genes, so that the gene has been renamed sag. 37 There is evidence that the gene sag, and consequently the super stimulus eliminate clones of T cells, can depress the immune system and reduce immune surveillance tumorales.40 cell biology of this virus has caused the interest in finding similar gene products in other retroviral infections, speculated that the pathogenesis of AIDS engage a superantigen effect very similar.40
Sheep and goats are the only domestic species so far described as susceptible to epithelial malignancies associated with retroviral infections. Virus-like morphology and biochemistry of type D simian retroviruses have been detected in lung and nasal carcinomas in small ruminants. 41,42,43 carcinoma sheep lung (CPO, jaagsiekte, pulmonary adenomatosis) is a highly prevalent disease in many countries around the world and the leading cause of death in sheep in Peru. 42.44 Adenocarcinoma similar passages related to retroviral infection have recently been described in Europe. 43 The retrovirus has a predilection for secretory epithelial cells with proliferative capacity, the viral infection in the lung alveolar epithelial cells transformed (type II pneumocytes) and terminal bronchiolar cells (Clara cells) and in the sinuses of the tubular glands of the mucosa Bowman in the olfactory turbinates. 45.46 The clinical descriptions and experimental transmissions of the CPO has sido ampliamente estudiada. El virus se transmite fundamentalmente por vía aerógena y son de curso clínico muy lento, 41,42 pero animales recién nacidos reproducen experimentalmente la enfermedad en períodos muy cortos. La alta susceptibilidad a inoculaciones experimentales de animales neonatos y corderos jóvenes permite especular que el virus pueda transmitirse en etapas biológicas muy tempranas y no exclusivamente por vías respiratorias. 47 El CPO es una enfermedad en la que la biología molecular ha elucidado al agente etiológico, sin necesidad de aislar exitosamente el virus en el laboratorio. 48 Esta inhabilidad ha hecho que se desconozcan detalles acerca de la patobiología de la enfermedad. Poco a nada se conoce sobre el mecanismo of malignant transformation, it is not known which cells are used in viral replication during the initial phase of infection. Recent studies show that clinical and experimental animals with retrovirus patients suffering from severe lymphopenia CPO. mainly associated with dramatic decreases in helper T lymphocytes (CD4). 48 animals studied also showed signs of inmunodesregulación such as significant increase in number and proportion of B cells, hypergammaglobulinemia, reduced thymus weight associated with lymphoid hypoplasia. 48 These findings suggest that the virus would be using lymphocytes as a possible viral replication cells trigger on other things in boxes immunosuppression. These studies is found, the retrovirus of CPO would have a biological similarity to murine retrovirus, in the ability of lymphoid cells used as carriers and spreaders of the infection would end by totally unknown mechanisms in lung carcinomas.
Al found that a wide variety of domestic animals and wildlife were susceptible to retroviral infection means that many researchers began to doubt the absence of similar viruses in humans. Thus begins an intense search of viral isolates in certain chronic diseases. The first success comes from laboratory of Robert Gallo, who can identify the first human retrovirus associated with T cell leukemia virus (human T-lymphotropic virus-type I). 49 The success was achieved due to the prior discovery of certain growth factors (interleukin 2) necessary to extend cultivation of lymphoid cells in vitro, and be able to detect retroviral replication. 49 Subsequently, thanks to a huge investment without precedent in medical history, the French group led by Montagnier and Gallo led by American, able to isolate the causative agent of the dreaded disease of AIDS. 50.51 The isolated virus has an extraordinary morphological and biochemical similarity with the virus of sheep "Maedi" 50.51 After many decades, not only proves the human M their susceptibility to infection by retroviruses, but also to isolate a non-oncogenic retroviruses but highly pathogenic (human lentivirus). These findings are finally able to convince the scientific community about the association of retroviruses and chronic processes, and attract many researchers now busily trying to find similar players in many chronic diseases and / or consumantes diseases such as multiple sclerosis, rheumatoid arthritis certain leukemias and lymphomas in humans.
In an effort to identify the best animal model that can answer the big questions about the difficult biology of the HIV virus, have intensified losestudiosen animals with lentiviral spontaneous disease. 52 Studies on animal pathogenicity of lentiviruses shows that most of these viruses are able to stay in the host using many factors, but primarily infect immunologically privileged cells such as lymphocytes and macrophages mainly. 53 The virus using lymph cells as sites of viral replication, evade immune destruction and manage to remain in the infected organism for prolonged periods. 53 The phenomenon of persistence of these viruses depends on the perfect interplay virus / cell. By infecting cell line monocytes / macrophages not only make use of biological and physiological properties of these cells, but are used as the principal disseminators of infection throughout the body of the animal. By this mechanism of spread, called "Trojan horse", infected cells travel throughout the body carrying virus hidden in certain physiological conditions expected to travel abroad and infect other cells and initiate disease in different areas of the body . 54 This mechanism also explains the different pathological manifestations such as chronic lymphoid proliferative pneumonia, nonsuppurative encephalitis, mastitis proliferative lymphoid, and arthritic lesions observed in a single lentiviral infection in small ruminants. 54 In these different organs produce the critical contact between the virus carrier cells (monocytes / macrophages infected) and non-lymphoid cells susceptible to cytopathic effect (cell death) with pathological consequences.
Recent studies also have begun to elucidate the mechanism of transmission in some retroviral diseases in domestic animals. Small ruminant lentiviruses are transmitted from infected mother to newborn animals mainly through colostrum and milk. 55 In bovine leukemia virus infections and equine infectious anemia The virus is mainly transmitted through infected blood inoculations. 56 In these diseases, infecting inoculations are performed by blood-sucking insects and / or through infected needles commonly seen in veterinary practice for vaccination group and / or blood samples for diagnosis. 56 The producer of the retrovirus feline leukemia, in addition to using lymphoid cells (lymphocytes and macrophages) to viral replication, using digestive tract epithelial cells, and during the final stage of infection, salivary gland cells. 57 The diverse causes the cell tropism of feline leukemia virus is transmitted by feces and salivary secretions. 57 All these studies demonstrate the tremendous capacity of the retrovirus to infect have more than one type of cells and especially a variety of transmission mechanisms.
parallel, studies in humans have begun to demonstrate that the HIV virus has a very similar biology to that observed in animals. Infection with the AIDS virus mainly produces severe selective lytic destruction of T cells (immune), but also capable of infecting cells of the line monocyte / macrophage. 58 During the course of the disease of AIDS is increasingly observed in the digestive tract infections, respiratory and nervous (AIDS dementia). Some 58 patients and people with AIDS especially children, show predominant lesions, respiratory (pneumonia proliferative lymphoid) of tremendous similarity respiratory syndrome (maedi) of sheep. 58 Similarly, the human nervous symptoms appear to be products of infected macrophage infiltration of the brain that leads to neuronal degeneration due to release of inflammatory products. This mechanism is identical to that observed in ovine lentivirus infection of the brain in degenerative brain boxes (Visna). 60 Similar to that reported in some retroviruses in animals have shown that the AIDS virus is transmitted, both through the blood through breast milk from infected mothers to newborns. 58 Finally, molecular studies show that retrovirus isolated from animals have tremendous capacity to mutate genetically very similar to the AIDS virus. 61 This large antigenic variability is observed in the virus producer of equine infectious anemia, where the constant mutation causes infected animals suffering from anemia as a result of periodic cyclic recurrence of variant strains in the infected animal. 61
On the other hand, in an effort to clarify the focus of origin of the AIDS virus in humans producer, have intensified research on retroviruses in living animals wildlife, especially nonhuman primates. 62 Virus molecular biology related and similar to HIV were first isolated in Asian macaques bred in captivity suffering from leukemia / lymphoma (simian lentivirus). 62.63 Similar isolates were subsequently reported in African green monkeys, mangabeys and macaques Asian, despite 30% of African green monkeys from Central Africa are positive carriers of infection apparently are not associated with any disease boxes. 64 The investigation of the virus in monkeys showed the existence of genetic similarity tremendous strains of HIV virus isolated from central Africa (HIV-2). Such data allowed to deduce that the Simian virus is the closest to the human virus and speculate on the possible source of origin of the AIDS virus. 65 The retrovirus of the Apes, like humans, show a high genetic variability, but show different evolutionary behavior. The strains that cause disease in monkeys of African origin immunodeficiency produce boxes in Asian macaques held in captivity. 65 It is not known the answer to this apparent ambivalence, but it is speculated that this is the product of genetic evolutionary experience. African apes appear to have evolved into a coexistence simian virus non-pathogenic, producing boxes instead of AIDS in Asian monkeys. In this scheme, it is hard to imagine that certain genetic mutations have occurred first in the wild variant capable of infecting humans and that through continuous and high passes between human populations to produce another high-pathogenic variant that well explain the onset of a pandemic of the century. 66
A variety of domestic animals, laboratory and wild animals are susceptible to infection by retroviruses. Infections are chronic and the injury or illness product of these infections vary tremendously. In some species of animals live in harmony virus causing minor injuries and many other causes of injuries are degenerative emaciantes, tumor or severe AIDS-like immunosuppressive described in humans. By showing that humans are susceptible to retroviral infection, there was an unusual interest in the retrovirology that led to the rediscovery of pioneering studies, the scientific recognition to some researchers, and the resurgence of interest in the study of similar diseases in many animal species . There are many achievements during this period, but the knowledge of the duck-retroviral biology has elucidated that the virus uses cells of the immune system preferentially, and the ability of certain specific genes lies in oncornavirus called oncogenes. On the other hand, the discovery of these oncogenes has helped identify similar genes responsible for controlling harmonious development, proliferation and cell differentiation (protoncogenes), but mostly that mutations in these genes may trigger malignant processes. Are many stages to be clarified for the full understanding of retroviral biology, but progress on understanding the molecular pathology conducive to developing the long-awaited vaccine to help control retroviral infections in humans and animals.
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Livestock Research 6 (1) January-June 1993
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