Avtor/Urednik		Tozon, Nataša
Naslov		Mačji virus imunske pomanjkljivosti - patološkohistološke spremembe na ledvicah okuženih mačk
Prevedeni naslov		Feline immunodeficiency virus (FIV) - histologic alterations in kidney in infected cats
Tip		članek
Vir		Med Razgl
Vol. in št.		Letnik 39, št. Suppl 4
Leto izdaje		2000
Obseg		str. 127-35
Jezik		slo
Abstrakt		Background. In our research we would like to determine possible histological alterations in kidney caused by feline immunodeficiency virus (FIV). Specific pathogen free (SPF) cats were used to exclude the influence of other pathogen agents. Methods. 38 cats were examined. 12 were naturally infected (group A) and 23 were SPF cats. Among them 10 were infected with the Petaluma viral isolate which we grew from approximately 160 passages on cell cultures (group B1), 6 with Pisa M2 viral isolate which was gained on live animals (group B2), 6 with both viral isolates (group B3) and 4 were SPF serologically negative cats as a control group (Bk). The results of the ELISA rapid test were confirmed in all cases with Western blot and polymerase chain reaction (PCR) techniques. Results. With histological examination of kidney tissue slices, we discovered the changes in the mesangium, the extent of the mesangium in varius dimensions and in 4 cases also mesan- gioproliferative glomerulonephritis. The pathological changes of kidney tissue do not increase histologically with respect to the time after innoculation. Extensive histological damage was discovered in the B2 group (Pisa M2). In naturally infected cats amyloidosis of glomerules and tubules, interstitial nephritis and glomerulosclerosis were also detected. Discussion and conclusion. The immune mechanisms that are responsible for histological changes in kidneys, especially in the mesangium, are a function of cytotoxic antibodies, T cytotoxic cells and the alternative mechanism of complement activation. Glomerulosclerosis, amyloidosis and interstitial nephritis are most likely caused by chronic function of the virus, either direct or through immune mechanisms.
Izvleček		Izhodišča. Z raziskavo smo želeli ugotoviti, ali mačji virus imunske pomanjkljivosti povzroča spremembe na ledvicah oziroma za katere spremembe na ledvicah je odgovoren, kar nakazujejo avtorji nekaterih študij. Za namen raziskave smo uporabili eksperimentalno okužene SPF-mačke, pri katerih lahko izključimo vpliv oportunističnih in sekundarnih okužb. Metode. V naši raziskavi smo pregledovali histološke rezine ledvic 38 mačk: 12 naravno okuženih (skupina A) in 23 poskusno okuženih SPF-mačk, 10 okuženih z virusnim izolatom Petaluma, pridobljenim s približno 160 pasažami na celični kulturi (skupina B1), 6 okuženih z izolatom Pisa M2, pasiranim na živih živalih (skupina B2), 6 okuženih z obema izolatoma (skupina B3), in 4 SPF-serološko negativne mačke kot kontrolna skupina (skupina Bk). V vseh primerih smo okužbo ugotavljali s hitrimi testi z metodo ELISA in jo potrdili z metodama Western-blot in verižno rekacijo s polimerazo. Rezultati. S histološkim pregledom rezin ledvičnega tkiva smo pri vseh SPF-mačkah ugotovili spremembe v mezangiju: razširitev le-tega v različnem obsegu, v 4 primerih pa je šlo za mezangioproliferativni glomerulonefritis. Bolezenske spremembe ledvičnega tkiva se histološko, glede na čas po inokulaciji, ne stopnjujejo. Najobsežnejše histološke poškodbe je bilo mogoče ugotoviti pri skupini B2 (Pisa M2). Pri naravno okuženih mačkah smo ugotovili še amiloidozo glomerulov in tubulov, intersticijski nefritis in glomerulosklerozo. Zaključki. Menimo, da bi bili lahko za bolezenske spremembe na ledvicah, predvsem v mezangiju odgovorni imunski mehanizmi: delovanje citotoksičnih protiteles oziroma specifičnih citotoksičnih celic T in mehanizem aktivacije komplementa po alternativni poti. Glomeruloskleroza, amiloidoza in intersticijski nefritis so verjetno posledica kroničnega delovanja viru- sa, bodisi neposredno ali prek imunskih mehanizmov.
Deskriptorji		IMMUNODEFICIENCY VIRUS, FELINE KIDNEY DISEASES CATS