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Articoli di riviste sul tema "Feline immunodeficiency virus"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 31 gennaio 2023

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1

Hosie, Margaret, Andrew Sparkes e Cherida Hopper. "Feline immunodeficiency virus". In Practice 11, n. 3 (maggio 1989): 87–95. http://dx.doi.org/10.1136/inpract.11.3.87.

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2

ROBINSON, WF, SE SHAW, R. ALEXANDER e I. ROBERTSON. "Feline immunodeficiency virus". Australian Veterinary Journal 67, n. 8 (agosto 1990): 278–80. http://dx.doi.org/10.1111/j.1751-0813.1990.tb07796.x.

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3

Bęczkowski, Paweł M., e Julia A. Beatty. "Feline Immunodeficiency Virus". Advances in Small Animal Care 3, n. 1 (novembre 2022): 145–59. http://dx.doi.org/10.1016/j.yasa.2022.05.007.

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4

Legendre, A. M. "Feline leukemia virus & feline immunodeficiency virus". Veterinary Quarterly 18, sup1 (aprile 1996): 38–39. http://dx.doi.org/10.1080/01652176.1996.9694668.

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5

Michelle Willis, A. "Feline Leukemia Virus and Feline Immunodeficiency Virus". Veterinary Clinics of North America: Small Animal Practice 30, n. 5 (settembre 2000): 971–86. http://dx.doi.org/10.1016/s0195-5616(00)05001-4.

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6

SHIMOJIMA, Masayuki. "Feline immunodeficiency virus tropism". Uirusu 57, n. 1 (2007): 75–82. http://dx.doi.org/10.2222/jsv.57.75.

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7

Pedersen, N. C., J. K. Yamamoto, T. Ishida e H. Hansen. "Feline immunodeficiency virus infection". Veterinary Immunology and Immunopathology 21, n. 1 (maggio 1989): 111–29. http://dx.doi.org/10.1016/0165-2427(89)90134-7.

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8

Miyazawa, Takayuki. "Infections of feline leukemia virus and feline immunodeficiency virus". Frontiers in Bioscience 7, n. 1-3 (2002): d504. http://dx.doi.org/10.2741/miyazawa.

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Miyazawa, Takayuki. "Infections of feline leukemia virus and feline immunodeficiency virus". Frontiers in Bioscience 7, n. 4 (2002): d504–518. http://dx.doi.org/10.2741/a791.

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10

Parry, Bruce W., Steven A. Holloway e Michael J. Studdert. "Diagnosis of Feline Leukemia Virus and Feline Immunodeficiency Virus Infections". Veterinary Clinics of North America: Small Animal Practice 19, n. 4 (luglio 1989): 719–27. http://dx.doi.org/10.1016/s0195-5616(89)50080-9.

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11

ZWIJNENBERG, R. "Feline immunodeficiency virus vaccine issues". Australian Veterinary Journal 83, n. 4 (aprile 2005): 215. http://dx.doi.org/10.1111/j.1751-0813.2005.tb11652.x.

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BEATTY, JA, VRD BARRS, CR O'BRIEN, SF FOSTER, DJ FOSTER, AL LITSTER e R. MALIK. "Feline immunodeficiency virus vaccine issues". Australian Veterinary Journal 83, n. 1-2 (gennaio 2005): 53. http://dx.doi.org/10.1111/j.1751-0813.2005.tb12193.x.

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13

Frey, Susan C. S., Edward A. Hoover e James I. Mullins. "Feline Immunodeficiency Virus Cell Entry". Journal of Virology 75, n. 11 (1 giugno 2001): 5433–40. http://dx.doi.org/10.1128/jvi.75.11.5433-5440.2001.

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ABSTRACT The process of feline immunodeficiency virus (FIV) cell entry was examined using assays for virus replication intermediates. FIV subtype B was found to utilize the chemokine receptor CXCR4, but not CCR5, as a cellular receptor. Zidovudine blocked formation of late viral replication products most effectively, including circular DNA genome intermediates. Our findings extend the role of CXCR4 as a primary receptor for CD4-independent cell entry by FIV.
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14

Yamamoto, Janet K., Ruiyu Pu, Eiji Sato e Tsutomu Hohdatsu. "Feline immunodeficiency virus pathogenesis and development of a dual-subtype feline-immunodeficiency-virus vaccine". AIDS 21, n. 5 (marzo 2007): 547–63. http://dx.doi.org/10.1097/qad.0b013e328013d88a.

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15

Andersen, Philip R., e Phyllis Tyrrell. "Feline immunodeficiency virus diagnosis after vaccination". Animal Health Research Reviews 5, n. 2 (dicembre 2004): 327–30. http://dx.doi.org/10.1079/ahr200493.

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AbstractPrior to the widespread use of vaccination for the control of feline immunodeficiency virus (FIV) infection, diagnosis was made by the detection of antibodies against FIV. A number of commercial animal side tests perform quite well for this determination, with positive predictive values between 91 and 100% and negative predictive values between 96 and 100%. Furthermore, results of these tests could be confirmed by western blot analysis of FIV test-positive sera. Currently, a killed whole virus FIV vaccine has been made available to practitioners. Vaccinated cats seroconvert by ELISA and western blot, making presently available diagnostic tests, which rely on antibody detection, useless in cats after vaccination. The advisory panels of the American Association of Feline Practitioners and Academy of Feline Medicine both recommend testing for feline leukemia virus antigen and FIV antibody before vaccination.
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16

González, Roger, Cesar Britez, Ynes Bazán, Maria José Caballero, Edith Maldonado, Tania Bendlin e Estefania Alvarenga. "Association of the feline gingivostomatitis complex with the feline immunodeficiency virus and the feline leukemia virus". Compendio de Ciencias Veterinarias 12, n. 1 (30 giugno 2022): 20–25. http://dx.doi.org/10.18004/compend.cienc.vet.2022.12.01.20.

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17

Ramsauer, Sandra, Gert Bay, Marina Meli, Regina Hofmann-Lehmann e Hans Lutz. "Seroprevalence of Selected Infectious Agents in a Free-Ranging, Low-Density Lion Population in the Central Kalahari Game Reserves in Botswana". Clinical and Vaccine Immunology 14, n. 6 (25 aprile 2007): 808–10. http://dx.doi.org/10.1128/cvi.00307-06.

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ABSTRACT Twenty-one free-ranging Central Kalahari lions (Panthera leo) exhibited a high prevalence rate of feline herpesvirus (100%) and feline immunodeficiency virus (71.4%). Canine distemper virus and feline calicivirus occurred with a low prevalence. All individuals tested negative for feline coronavirus, feline parvovirus, feline leukemia virus, Ehrlichia canis, and Anaplasma phagocytophilum.
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18

Teng, Ching Sung. "Induction of feline immunodeficiency syndrome by feline leukemia virus". Aids 4, n. 12 (dicembre 1990): 1219–24. http://dx.doi.org/10.1097/00002030-199012000-00006.

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19

Kanzaki, Luis Isamu Barros. "Feline immunodeficiency virus: a concise review". Frontiers in Bioscience 9, n. 1-3 (2004): 370. http://dx.doi.org/10.2741/1235.

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20

Teixeira, Bruno M., Mitika K. Hagiwara, Juliano C. M. Cruz e Margaret J. Hosie. "Feline Immunodeficiency Virus in South America". Viruses 4, n. 3 (14 marzo 2012): 383–96. http://dx.doi.org/10.3390/v4030383.

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21

Saenz, D. T., R. Barraza, N. Loewen, W. Teo e E. M. Poeschla. "Feline Immunodeficiency Virus-Based Lentiviral Vectors". Cold Spring Harbor Protocols 2012, n. 1 (22 dicembre 2011): pdb.ip067579. http://dx.doi.org/10.1101/pdb.ip067579.

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22

O'NEIL, LYNNE L., MARY JO BURKHARD, LAURI J. DIEHL e EDWARD A. HOOVER. "Vertical Transmission of Feline Immunodeficiency Virus". AIDS Research and Human Retroviruses 11, n. 1 (gennaio 1995): 171–82. http://dx.doi.org/10.1089/aid.1995.11.171.

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23

O'NEIL, LYNNE L., MARY JO BURKHARD, LESLIE A. OBERT e EDWARD A. HOOVER. "Regression of Feline Immunodeficiency Virus Infection". AIDS Research and Human Retroviruses 13, n. 8 (20 maggio 1997): 713–18. http://dx.doi.org/10.1089/aid.1997.13.713.

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24

Hartmann, K. "Feline immunodeficiency virus infection: an overview". Veterinary Journal 155, n. 2 (marzo 1998): 123–37. http://dx.doi.org/10.1016/s1090-0233(98)80008-7.

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25

Gaskell, C. J. "Feline immunodeficiency virus—Aids in cats?" British Veterinary Journal 148, n. 5 (settembre 1992): 373–74. http://dx.doi.org/10.1016/0007-1935(92)90024-u.

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26

Bennett, M., e N. R. Smyth. "Feline immunodeficiency virus: A brief review". British Veterinary Journal 148, n. 5 (settembre 1992): 399–412. http://dx.doi.org/10.1016/0007-1935(92)90027-x.

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27

MIYAZAWA, Takayuki, e Takeshi MIKAMI. "Biological Nature of Feline Immunodeficiency Virus." Journal of Veterinary Medical Science 55, n. 4 (1993): 519–26. http://dx.doi.org/10.1292/jvms.55.519.

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28

Olmsted, R. A., A. K. Barnes, J. K. Yamamoto, V. M. Hirsch, R. H. Purcell e P. R. Johnson. "Molecular cloning of feline immunodeficiency virus." Proceedings of the National Academy of Sciences 86, n. 7 (1 aprile 1989): 2448–52. http://dx.doi.org/10.1073/pnas.86.7.2448.

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29

Hosie, Margaret J., Robert Osborne, George Reid, James C. Neil e Oswald Jarrett. "Enhancement after feline immunodeficiency virus vaccination". Veterinary Immunology and Immunopathology 35, n. 1-2 (dicembre 1992): 191–97. http://dx.doi.org/10.1016/0165-2427(92)90131-9.

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30

Miyazawa, T., K. Tomonaga, Y. Kawaguchi e T. Mikami. "The genome of feline immunodeficiency virus". Archives of Virology 134, n. 3-4 (settembre 1994): 221–34. http://dx.doi.org/10.1007/bf01310563.

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31

Alves. "Occurrence of Feline Immunodeficiency Virus and Feline Leukemia Virus Infection in Cats". American Journal of Animal and Veterinary Sciences 6, n. 3 (1 marzo 2011): 125–29. http://dx.doi.org/10.3844/ajavsp.2011.125.129.

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32

Hartmann, Katrin. "Clinical aspects of feline immunodeficiency and feline leukemia virus infection". Veterinary Immunology and Immunopathology 143, n. 3-4 (ottobre 2011): 190–201. http://dx.doi.org/10.1016/j.vetimm.2011.06.003.

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33

Sprague, Wendy S., Melissa Robbiani, Paul R. Avery, Kevin P. O'Halloran e Edward A. Hoover. "Feline immunodeficiency virus dendritic cell infection and transfer". Journal of General Virology 89, n. 3 (1 marzo 2008): 709–15. http://dx.doi.org/10.1099/vir.0.83068-0.

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Abstract (sommario):
Feline immunodeficiency virus (FIV) interacts with dendritic cells (DC) during initiation of infection, but whether DC support or transfer FIV infection remains unclear. To address this issue, we studied the susceptibility of feline myeloid DC to FIV infection and assessed potential transfer of infection from DC to CD4+ T cells. FIV was detected in membrane-bound vesicles of DC within 2 h of inoculation, although only low concentrations of FIV DNA were found in virus-exposed isolated DC. Addition of resting CD4+ T cells increased viral DNA levels; however, addition of activated CD4+ T cells resulted in a burst of viral replication manifested by FIV p27 capsid antigen generation. To determine whether transfer of FIV infection required productively infected DC (vs virus bound to DC but not internalized), virus-exposed DC were cultured for 2 days to allow for degradation of uninternalized virus and initiation of infection in the DC, then CD4+ T blasts were added. Infection of T cells remained robust, indicating that T-cell infection is likely to be mediated by de novo viral infection of DC followed by viral transfer during normal DC/T-cell interactions. We conclude that feline DC support restricted FIV infection, which nevertheless is sufficient to efficiently transfer infection to susceptible T cells and trigger the major burst of viral replication. Feline DC/FIV/T-cell interactions (similar to those believed to occur in human immunodeficiency virus and simian immunodeficiency virus infections) highlight the means by which immunodeficiency-inducing lentiviruses exploit normal DC/T-cell interactions to transfer and amplify virus infection.
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34

Rocha, Mariana Araújo, Reginaldo Pereira Sousa Filho, Keytyanne Oliveira Sampaio e Marina Gabriela Monteiro Carvalho Mori da Cunha. "Seroprevalence of feline immunodeficiency virus and feline leukemia virus in domestic cats of Fortaleza, Ceará". Brazilian Journal of Veterinary Research and Animal Science 56, n. 1 (1 luglio 2019): e146687. http://dx.doi.org/10.11606/issn.1678-4456.bjvras.2019.146687.

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Feline Immunodeficiency Virus (FIV) and Feline Leukemia Virus (FeLV) are important etiologic agents of immunosuppressive diseases in felines. The objective of the present study was to determine the prevalence of these retroviruses in domestic cats in Fortaleza, Ceará and the epidemiological factors associated with these infections. Between 2015 and 2016, 138 blood samples were collected and tested for FIV and FeLV by the enzyme immunoadsorption assay (ELISA). Parameters such as breed, gender, age, reproductive status, multi-cat environment, outdoor access and clinical manifestations were evaluated. The results showed that 12.32% were positive for FIV, 5.80% for FeLV and 1.45% for co-infection (FIV/FeLV). FIV+ animals were mostly mixed breed, neutered male adult cats, with indoor lifestyle and living in a multi-cat household. The most common clinical manifestation observed was disorders of the oral cavity. Factors found to increase the risk for FeLV seropositivity include mixed breed, young, spayed female cats, indoor lifestyle living in a multi-cat household were the most common epidemiological factors observed. The most common clinical manifestation was anorexia and apathy. The prevalence of these viruses were relatively high, compared with other region of Brazil. This study demonstrated that mixed breed, castrated, multi-cat environment and indoor lifestyle animals are of greater relevance for FIV and FeLV infection diseases. Factors related to cat demographics and health such as age, sex and type of household are important predictors for seropositive status to FeLV or FIV in Fortaleza. High prevalence of FeLV or FIV observed in our study is of concern, in view of the immunosuppressive potential of the two pathogens.
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35

SOMA, Takehisa, Ryusaku YOSHIUCHI, Koichiro KITAO, Yoshihisa HONDA, Nobuyuki YAMASHITA, Naoyuki ISHIKAWA, Hiroki YAMAMOTO e Taisei HOSOIDO. "Prevalence of Feline Immunodeficiency Virus, Feline Leukemia Virus, and Feline Coronavirus Infections in 140 Ownerless Kittens". Journal of the Japan Veterinary Medical Association 71, n. 10 (20 ottobre 2018): 577–80. http://dx.doi.org/10.12935/jvma.71.577.

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36

Hosie, Margaret J., Daniela Pajek, Ayman Samman e Brian J. Willett. "Feline Immunodeficiency Virus (FIV) Neutralization: A Review". Viruses 3, n. 10 (13 ottobre 2011): 1870–90. http://dx.doi.org/10.3390/v3101870.

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37

Zielonka, Jörg, e Carsten Münk. "Cellular Restriction Factors of Feline Immunodeficiency Virus". Viruses 3, n. 10 (21 ottobre 2011): 1986–2005. http://dx.doi.org/10.3390/v3101986.

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38

Mohammadi, Hakimeh, e Dorothee Bienzle. "Pharmacological Inhibition of Feline Immunodeficiency Virus (FIV)". Viruses 4, n. 5 (27 aprile 2012): 708–24. http://dx.doi.org/10.3390/v4050708.

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39

Shelton, GH, ML Linenberger, CK Grant e JL Abkowitz. "Hematologic manifestations of feline immunodeficiency virus infection". Blood 76, n. 6 (15 settembre 1990): 1104–9. http://dx.doi.org/10.1182/blood.v76.6.1104.1104.

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Abstract (sommario):
Abstract Studies were done on 53 cats with community-acquired infection with the feline immunodeficiency virus (FIV) to determine if hematologic abnormalities were comparable with those observed in patients seropositive for the human immunodeficiency virus (HIV). Nine cats were asymptomatic, 24 had clinical symptoms equivalent to AIDS-related complex (ARC), and 20 had AIDS-like disease. Hematologic abnormalities were detected in 75% (40 of 53) of FIV-seropositive cats, and multiple concurrent cytopenias were common. Anemia, lymphopenia, neutropenia, and thrombocytopenia occurred in 36%, 53%, 34%, and 8% of FIV- seropositive cats, respectively. Cytopenias were seen only in symptomatic (ARC or AIDS) cats. The occurrence of cytopenias and the distribution of clinical stages were similar in cats with concurrent feline leukemia virus (FeLV) infection and those with FIV alone, suggesting that these abnormalities were a direct consequence of FIV infection. In addition, abnormalities were noted in 72% of marrows from symptomatic cats and included hyperplasia of individual cell lineages and dysmorphic features. Our results demonstrate that the hematologic manifestations of FIV infection are strikingly similar to those reported in HIV-seropositive patients. Thus, FIV infection in cats is an excellent animal model to study the pathogenesis of blood and marrow abnormalities in AIDS, as well as to evaluate the hematologic toxicities of drug therapies.
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40

Shelton, GH, ML Linenberger, CK Grant e JL Abkowitz. "Hematologic manifestations of feline immunodeficiency virus infection". Blood 76, n. 6 (15 settembre 1990): 1104–9. http://dx.doi.org/10.1182/blood.v76.6.1104.bloodjournal7661104.

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Abstract (sommario):
Studies were done on 53 cats with community-acquired infection with the feline immunodeficiency virus (FIV) to determine if hematologic abnormalities were comparable with those observed in patients seropositive for the human immunodeficiency virus (HIV). Nine cats were asymptomatic, 24 had clinical symptoms equivalent to AIDS-related complex (ARC), and 20 had AIDS-like disease. Hematologic abnormalities were detected in 75% (40 of 53) of FIV-seropositive cats, and multiple concurrent cytopenias were common. Anemia, lymphopenia, neutropenia, and thrombocytopenia occurred in 36%, 53%, 34%, and 8% of FIV- seropositive cats, respectively. Cytopenias were seen only in symptomatic (ARC or AIDS) cats. The occurrence of cytopenias and the distribution of clinical stages were similar in cats with concurrent feline leukemia virus (FeLV) infection and those with FIV alone, suggesting that these abnormalities were a direct consequence of FIV infection. In addition, abnormalities were noted in 72% of marrows from symptomatic cats and included hyperplasia of individual cell lineages and dysmorphic features. Our results demonstrate that the hematologic manifestations of FIV infection are strikingly similar to those reported in HIV-seropositive patients. Thus, FIV infection in cats is an excellent animal model to study the pathogenesis of blood and marrow abnormalities in AIDS, as well as to evaluate the hematologic toxicities of drug therapies.
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41

Allison, Robin W., e Edward A. Hoover. "Covert Vertical Transmission of Feline Immunodeficiency Virus". AIDS Research and Human Retroviruses 19, n. 5 (maggio 2003): 421–34. http://dx.doi.org/10.1089/088922203765551764.

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42

Taylor, F. "Feline immunodeficiency virus and tests for HIV". Veterinary Record 130, n. 5 (1 febbraio 1992): 107. http://dx.doi.org/10.1136/vr.130.5.107-b.

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43

YAMAMOTO, JANET K., TAKIKO OKUDA, CHRISTOPHER D. ACKLEY, HARRY LOUIE, ERIN PEMBROKE, HOWARD ZOCHLINSKI, ROBERT J. MUNN e MURRAY B. GARDNER. "Experimental Vaccine Protection Against Feline Immunodeficiency Virus". AIDS Research and Human Retroviruses 7, n. 11 (novembre 1991): 911–22. http://dx.doi.org/10.1089/aid.1991.7.911.

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44

Cano-Ortiz, Lucía, Dennis Maletich Junqueira, Juliana Comerlato, Cristina Santos Costa, André Zani, Naila Blatt Duda, Caroline Tochetto et al. "Phylodynamics of the Brazilian feline immunodeficiency virus". Infection, Genetics and Evolution 55 (novembre 2017): 166–71. http://dx.doi.org/10.1016/j.meegid.2017.09.011.

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45

ISHIDA, Takuo, e Isamu TOMODA. "Clinical staging of feline immunodeficiency virus infection." Japanese Journal of Veterinary Science 52, n. 3 (1990): 645–48. http://dx.doi.org/10.1292/jvms1939.52.645.

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46

Teixeira, Bruno Marques, Sueli Akemi Taniwaki, Poliana Marisa Miranda Menezes, Ana Kétylla Ponte Prado Rodrigues, Andressa Nunes Mouta, Thiago Luiz Mendes Arcebispo, Gissandra Farias Braz et al. "Feline immunodeficiency virus in Northern Ceará, Brazil". Journal of Feline Medicine and Surgery Open Reports 5, n. 2 (luglio 2019): 205511691985911. http://dx.doi.org/10.1177/2055116919859112.

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Abstract (sommario):
ObjectivesThe objectives of this study were to confirm the prevalence of feline immunodeficiency virus (FIV) infection in domestic cats in the region north of Ceará, Brazil, and to determine the factors associated with infection and the major circulating subtypes of the virus in this area.MethodsSamples from 148 cats were collected and tested using anti-FIV antibody screening, with confirmation of positive results by PCR. Univariate analysis was performed considering the epidemiological characteristics and FIV status. Sequencing and phylogenetic analysis of the gag and pol genes were performed to confirm the FIV subtype.ResultsNine cats (6.1%) tested positive for FIV – one female (0.7%) and eight males (5.4%). Male cats were significantly more likely to be infected ( P <0.05). Phylogenetic analysis of gag and pol gene sequences indicated that the FIV isolates circulating in the study area belonged to subtype B.Conclusions and relevanceIn this study, we demonstrated a low prevalence for FIV in the northwest of Ceará, north-eastern Brazil. Male sex is a significant risk factor for FIV infection and the best predictive factor for FIV status. All isolates examined in this study clustered within subtype B, which is the predominant subtype in Brazil. This is the first report of genetic characterization of FIV in the state of Ceará, Brazil.
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47

Giannecchini, S., D. Matteucci, P. Mazzetti e M. Bendinelli. "Incubation time for feline immunodeficiency virus cultures." Journal of clinical microbiology 34, n. 8 (1996): 2036–38. http://dx.doi.org/10.1128/jcm.34.8.2036-2038.1996.

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48

Sparger, Ellen Elizabeth. "Current Thoughts on Feline Immunodeficiency Virus Infection". Veterinary Clinics of North America: Small Animal Practice 23, n. 1 (gennaio 1993): 173–91. http://dx.doi.org/10.1016/s0195-5616(93)50011-6.

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49

Luttge, Benjamin G., Miranda Shehu-Xhilaga, Dimiter G. Demirov, Catherine S. Adamson, Ferri Soheilian, Kunio Nagashima, Andrew G. Stephen, Robert J. Fisher e Eric O. Freed. "Molecular Characterization of Feline Immunodeficiency Virus Budding". Journal of Virology 82, n. 5 (19 dicembre 2007): 2106–19. http://dx.doi.org/10.1128/jvi.02337-07.

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Abstract (sommario):
ABSTRACT Infection of domestic cats with feline immunodeficiency virus (FIV) is an important model system for studying human immunodeficiency virus type 1 (HIV-1) infection due to numerous similarities in pathogenesis induced by these two lentiviruses. However, many molecular aspects of FIV replication remain poorly understood. It is well established that retroviruses use short peptide motifs in Gag, known as late domains, to usurp cellular endosomal sorting machinery and promote virus release from infected cells. For example, the Pro-Thr/Ser-Ala-Pro [P(T/S)AP] motif of HIV-1 Gag interacts directly with Tsg101, a component of the endosomal sorting complex required for transport I (ESCRT-I). A Tyr-Pro-Asp-Leu (YPDL) motif in equine infectious anemia virus (EIAV), and a related sequence in HIV-1, bind the endosomal sorting factor Alix. In this study we sought to identify and characterize FIV late domain(s) and elucidate cellular machinery involved in FIV release. We determined that mutagenesis of a PSAP motif in FIV Gag, small interfering RNA-mediated knockdown of Tsg101 expression, and overexpression of a P(T/S)AP-binding fragment of Tsg101 (TSG-5′) each inhibited FIV release. We also observed direct binding of FIV Gag peptides to Tsg101. In contrast, mutagenesis of a potential Alix-binding motif in FIV Gag did not affect FIV release. Similarly, expression of the HIV-1/EIAV Gag-binding domain of Alix (Alix-V) did not disrupt FIV budding, and FIV Gag peptides showed no affinity for Alix-V. Our data demonstrate that FIV relies predominantly on a Tsg101-binding PSAP motif in the C terminus of Gag to promote virus release in HeLa cells, and this budding mechanism is highly conserved in feline cells.
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Lafrado, Louis J., Charlene S. Dezzutti, Mark G. Lewis e Richard G. Olsen. "Immunodeficiency in latent feline leukemia virus infections". Veterinary Immunology and Immunopathology 21, n. 1 (maggio 1989): 39–46. http://dx.doi.org/10.1016/0165-2427(89)90128-1.

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