Relationship of Lymphoid Lesions to Disease Course in Mucosal Feline Immunodeficiency Virus Type C Infection

Obert, Leslie; Hoover, Edward A.

doi:10.1354/vp.37-5-386

Cited by 27 publications

(38 citation statements)

References 60 publications

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“…The rate of rectal FIV-B-2542 transmission in the present study, and in concurrent work in this laboratory (39), is approximately 50%. This rate appeared to be independent of the TCID, and in vivo passage of the virus via rectal inoculation did not appear to increase the ability of the virus pool to cross the rectal mucosa.…”

Section: Discussionsupporting

confidence: 61%

Gamma Interferon/Interleukin 10 Balance in Tissue Lymphocytes Correlates with Down Modulation of Mucosal Feline Immunodeficiency Virus Infection

Avery

Hoover

2004

J Virol

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Understanding the early cytokine response to lentiviral infections may be critical to the design of prevention and treatment strategies. By using the feline immunodeficiency virus (FIV) model, we have documented an interleukin 10 (IL10)-dominated response in lymphoid tissue CD4؉ and CD8 ؉ T lymphocytes within the first 4 weeks after mucosal FIV infection. This profile coincided with the period of high tissue viral replication. By 10 weeks postinfection, tissue viral levels decreased significantly, and gamma interferon (IFN␥) production in CD8 ؉ T cells had increased to restore the IL10/IFN␥ ratio to control levels. Concurrently, increased production of IL6 and viral RNA was detected in macrophages. These temporal associations of viral replication with cytokine balance in tissues suggest roles for IL10 in the permissive stage of infection and IFN␥ in the subsequent down modulation of lentiviral infection.

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Section: Discussionsupporting

confidence: 61%

Gamma Interferon/Interleukin 10 Balance in Tissue Lymphocytes Correlates with Down Modulation of Mucosal Feline Immunodeficiency Virus Infection

Avery

Hoover

2004

J Virol

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“…Viral RNA was demonstrated in formalin-fixed tissue sections using a FIV RNA in situ hybridization protocol described elsewhere [20]. DNA in situ hybridization was done by modifying the RNA in situ hybridization protocol to include a 90ЊC heat denaturation step for 30 s-3 min immediately after probe application.…”

Section: Methodsmentioning

confidence: 99%

Fetal Feline Immunodeficiency Virus Is Prevalent and Occult

Rogers

Hoover

2002

J INFECT DIS

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The feline model of human acquired immune deficiency syndrome, feline immunodeficiency virus (FIV), was used to model maternal-to-fetal human immunodeficiency virus type 1 (HIV-1) transmission. Fetuses were collected from cats infected with clade A FIV(Petaluma) (FIV-A-Pet) and clade C FIV(PaddyGammer) (FIV-C-Pgmr). Virus was detected by DNA polymerase chain reaction (PCR) and a quantitative RNA assay that used substitutional PCR. FIV in tissue sections was assayed by DNA and RNA in situ hybridization and immunohistochemistry. Viral DNA was detected in 67% and 92% of fetuses with FIV-A-Pet and FIV-C-Pgmr, respectively. A discordance was observed between placental and fetal FIV-A-Pet localization. FIV sequestration in fetal tissues was common without detectable virus in blood (occult infection). Viral RNA was not detected in amniotic fluid or fetal plasma. In situ assays demonstrated FIV DNA but neither RNA nor antigens in placentas and fetuses. If mother-to-offspring FIV infection reflects vertical HIV-1 transmission, fetal virus exposure is common and may be occult at term.

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“…Also, inoculation of a domestic cat with PBMC from a PLV-infected puma resulted in infection but no clinical signs, similar to observations we have made in this and other studies (39a, 51). Infections in domestic cats after experimental inoculation with FIV by oronasal, rectal, and vaginal routes have previously been described (12,39); however, the virulence of infection is independent of the route of exposure. The cats used in this study were from a different source than other studies which have characterized virulent FIV, suggesting that genetic background may have played a role in our observations.…”

Section: Vol 79 2005 Mucosal Lentiviral Challenge Control In Domestmentioning

confidence: 99%

Puma Lentivirus Is Controlled in Domestic Cats after Mucosal Exposure in the Absence of Conventional Indicators of Immunity

TerWee

Yactor

Sondgeroth

et al. 2005

J Virol

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A high percentage of free-ranging pumas (Felis concolor) are infected with feline lentiviruses (puma lentivirus, feline immunodeficiency virus Pco [FIV-Pco], referred to here as PLV) without evidence of disease. PLV establishes productive infection in domestic cats following parenteral exposure but, in contrast to domestic cat FIV, it does not cause T-cell dysregulation. Here we report that cats exposed to PLV oro-nasally became infected yet rapidly cleared peripheral blood mononuclear cell (PBMC) proviral load in the absence of a correlative specific immune response. Two groups of four specific-pathogen-free cats were exposed to PLV via the mucosal (oro-nasal) or parenteral (i.v.) route. All animals were PBMC culture positive and PCR positive within 3 weeks postinfection and seroconverted without exhibiting clinical disease; however, three or four oro-nasally infected animals cleared circulating proviral DNA within 3 months. Antibody titers reached higher levels in animals that remained persistently infected. PLV antigen-induced proliferation was slightly greater in mucosally inoculated animals, but no differences were noted in cytotoxic T-lymphocyte responses or cytokine profiles between groups. The distribution of virus was predominantly gastrointestinal as opposed to lymphoid in all animals in which virus was detected at necropsy. Possible mechanisms for viral clearance include differences in viral fitness required for crossing mucosal surfaces, a threshold dose requirement for persistence, or an undetected sterilizing host immune response. This is the first report of control of a productive feline or primate lentivirus infection in postnatally exposed, seropositive animals. Mechanisms underlying this observation will provide clues to containment of immunodeficiency disease and could prompt reexamination of vaccine-induced immunity against human immunodeficiency virus and other lentiviruses.

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Relationship of Lymphoid Lesions to Disease Course in Mucosal Feline Immunodeficiency Virus Type C Infection

Cited by 27 publications

References 60 publications

Gamma Interferon/Interleukin 10 Balance in Tissue Lymphocytes Correlates with Down Modulation of Mucosal Feline Immunodeficiency Virus Infection

Gamma Interferon/Interleukin 10 Balance in Tissue Lymphocytes Correlates with Down Modulation of Mucosal Feline Immunodeficiency Virus Infection

Fetal Feline Immunodeficiency Virus Is Prevalent and Occult

Puma Lentivirus Is Controlled in Domestic Cats after Mucosal Exposure in the Absence of Conventional Indicators of Immunity

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