@article{schwartz_mccrackin_schinazi_hill_vahlenkamp_tompkins_hartmann_2014, title={Antiviral efficacy of nine nucleoside reverse transcriptase inhibitors against feline immunodeficiency virus in feline peripheral blood mononuclear cells}, volume={75}, ISSN={["1943-5681"]}, DOI={10.2460/ajvr.75.3.273}, abstractNote={Abstract}, number={3}, journal={AMERICAN JOURNAL OF VETERINARY RESEARCH}, author={Schwartz, Anita M. and McCrackin, Mary Ann and Schinazi, Raymond F. and Hill, Peter B. and Vahlenkamp, Thomas W. and Tompkins, Mary B. and Hartmann, Katrin}, year={2014}, month={Mar}, pages={273–281} }
 @article{liu_hudson_tompkins_vahlenkamp_colby_rundle_meeker_2006, title={Cerebrospinal fluid is an efficient route for establishing brain infection with feline immunodeficiency virus and transfering infectious virus to the periphery}, volume={12}, ISSN={["1538-2443"]}, DOI={10.1080/13550280600889567}, abstractNote={Like human immunodeficiency virus (HIV), feline immunodeficiency virus (FIV) invades and infects the central nervous system (CNS) soon after peripheral infection. The appearance of viral RNA is particularly prominent in the cerebrospinal fluid (CSF), suggesting an efficient route of virus transfer across the blood-CSF barrier. This raises the concern whether this route can establish a stable viral reservoir and also be a source of virus capable of reseeding peripheral systems. To examine this possibility, 200 μl of cell-free NCSU1 FIV or FIV-infected choroid plexus macrophages (ChP-Mac) was directly injected into the right lateral ventricle of the brain. Negative controls were sham inoculated with uninfected ChP-Mac or virus-free culture supernatant and positive controls were infected systemically by intraperitoneal (i.p.) injection. Intracerebroventricular (i.c.v.) inoculation with cell-free FIV resulted in high levels of plasma FIV RNA detected as early as 1 to 2 weeks post inoculation in all cats. In each case, the plasma viremia preceded the detection of CSF viral RNA. Compared to i.p. cats, i.c.v. cats had 32-fold higher CSF viral loads, 8-fold higher ratios of CSF to plasma viral load, and a 23-fold greater content of FIV proviral DNA in the brain. No FIV RNA was detected in plasma or CSF from the cats inoculated with FIV-infected ChP-Mac but an acute inflammatory response and a slight suppression of the CD4+:CD8+ ratio were observed. These results indicate that free FIV circulating in the CSF promotes infection of the CNS and provides a highly efficient pathway for the transfer of infectious virus to the periphery.}, number={4}, journal={JOURNAL OF NEUROVIROLOGY}, author={Liu, Pinghuang and Hudson, Lola C. and Tompkins, Mary B. and Vahlenkamp, Thomas W. and Colby, Brenda and Rundle, Cyndi and Meeker, Rick B.}, year={2006}, month={Aug}, pages={294–306} }
 @article{liu_hudson_tompkins_vahlenkamp_meeker_2006, title={Compartmentalization and evolution of feline immunodeficiency virus between the central nervous system and periphery following intracerebroventricular or systemic inoculation}, volume={12}, ISSN={["1355-0284"]}, DOI={10.1080/13550280600889575}, abstractNote={The emergence of distinct neuropathogenic strains resulting from the adaptation and the unique evolution of human immunodeficiency virus (HIV) in the brain may contribute to the development of HIV-induced neurological diseases. In this study, the authors tracked early changes in virus evolution and compartmentalization between peripheral tissues and the central nervous system (CNS) after intracerebroventricular (i.c.v.) or intraperitoneal (i.p.) inoculation of animals with cell-free feline immunodeficiency virus (FIV). Using the FIV-NCSU1 envelope V3–V4 heteroduplex tracking assay (HTA), the authors observed a rapid compartmentalization of envelope variants between the CNS and periphery. Animals receiving the i.c.v. inoculation showed two peaks of viral RNA in the cerebrospinal fluid (CSF) with very different HTA patterns. Compared to the initial viral peak in CSF, the second peak showed an increased compartmentalization from plasma, reduced viral diversity, and more divergence from the proviral DNA in peripheral blood mononuclear cells (PBMCs) and the choroid plexus. In contrast, changes in plasma over the same time period were small. Different animals harbored different FIV DNA genotypes with varied regional compartmentalization within the brain. These results demonstrated that the virus within the CNS experienced a relatively independent but variable evolution from the periphery. Initial penetration of virus into the CSF facilitated the development of brain-specific reservoirs and viral diversification within the CNS.}, number={4}, journal={JOURNAL OF NEUROVIROLOGY}, author={Liu, Pinghuang and Hudson, Lola C. and Tompkins, Mary B. and Vahlenkamp, Thomas W. and Meeker, Rick B.}, year={2006}, month={Aug}, pages={307–321} }
 @article{vahlenkamp_tompkins_tompkins_2005, title={The role of CD4(+)CD25(+) regulatory T cells in viral infections}, volume={108}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2005.07.011}, abstractNote={Many virus infections result in the suppression of one or more functions of the immune system. Multiple mechanisms have been proposed to explain viral-induced immunosuppression, including an imbalance in the cellular Th1/Th2 or cytokine profile, induction of anergy, depletion of effector cells and most recently the activation of CD4+CD25+ regulatory T (T reg) cells. CD4+CD25+ T reg cells are a subset of circulating CD4+ T cells with suppressive properties. CD4+CD25+ T reg cells were first identified in mice as cells capable of maintaining self-tolerance by suppressing autoreactive T cells. This review focuses on interactions between CD4+CD25+ T reg cells and viral pathogens. Most cases in which CD4+CD25+ T reg cells participate in response to infection reported so far involve chronic or persistent viral infections. Examples have been growing recently and include members of different viral families including retroviridae, herpesviridae and picornaviridae. It is currently not known how microbes are recognized by CD4+CD25+ T reg cells and whether exoantigen-specific T reg cells are of the same lineage as self-reacting natural T reg cells or represent peripherally induced counterparts derived from CD4+CD25− T cells. The findings that T reg cells influence the functional immunity during viral infections, however, might indicate that, in some cases, virus-specific T reg cells not only influence immune pathology or prevent pathogen elimination but also can promote a generalized state of immunosuppression in vivo such that the host is more susceptible to secondary infections with other pathogens or has reduced resistance to tumors. Conceivably, the activities of T reg cells might be one of the contributing reasons why it has been difficult so far to produce effective vaccines against some persisting viral infections.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Vahlenkamp, TW and Tompkins, MB and Tompkins, WAF}, year={2005}, month={Oct}, pages={219–225} }
 @article{vahlenkamp_bull_dow_collisson_winslow_phadke_tompkins_tompkins_2004, title={B7(+)CTLA4(+) T cells engage in T-T cell interactions that mediate apoptosis: a model for lentivirus-induced T cell depletion}, volume={98}, ISSN={["0165-2427"]}, DOI={10.1016/j.vetimm.2003.12.006}, abstractNote={Apoptosis in lymph node (LN) T cells of feline immunodeficiency virus (FIV)-infected cats is associated with cells co-expressing B7.1 and B7.2 costimulatory molecules, and their ligand CTLA4. To study the possibility of B7.1/B7.2-CTLA4 mediated T-T interactions and the predicted induction of T cell apoptosis in vitro, costimulatory molecules were up-regulated on CD4+ and CD8+ T cells by mitogen stimulation. B7.1 expression on in vitro stimulated CD4+ and CD8+ cells increased within 24h; B7.2 and CTLA4 expression increased after 48-72 h. Apoptosis, as analyzed by terminal deoxynucleotidyl transferase (transferase nick end labeling, TUNEL)-based staining followed by three color flow cytometric analysis, correlated to the cells expressing B7 and/or CTLA4. Blocking experiments revealed that CD4+ and CD8+ T cell apoptosis could be significantly inhibited with anti-B7 antibodies. As FIV infection results in immune activation with a T cell phenotype similar to that of the in vitro activated T cells, the data support the hypothesis that the chronic expansion of B7+CTLA4+ LN T cells in infected cats allows for T-T cell interactions resulting in T cell depletion and eventually the development of AIDS.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Vahlenkamp, TW and Bull, ME and Dow, JL and Collisson, EW and Winslow, BJ and Phadke, AP and Tompkins, WAF and Tompkins, MB}, year={2004}, month={Apr}, pages={203–214} }
 @article{huebner_klein_muller_vahlenkamp_langbein_2004, title={Combined anti-retroviral therapy (CART) in a feline immunodeficiency virus (FIV)infected cat}, volume={49}, number={8}, journal={Kleintier-Praxis}, author={Huebner, J. and Klein, D. and Muller, E. and Vahlenkamp, T. W. and Langbein, I.}, year={2004}, pages={517-} }
 @article{vahlenkamp_tompkins_tompkins_2004, title={Feline immunodeficiency virus infection phenotypically and functionally activates immunosuppressive CD4(+)CD25(+) T regulatory cells}, volume={172}, ISSN={["1550-6606"]}, DOI={10.4049/jimmunol.172.8.4752}, abstractNote={Abstract}, number={8}, journal={JOURNAL OF IMMUNOLOGY}, author={Vahlenkamp, TW and Tompkins, MB and Tompkins, WAF}, year={2004}, month={Apr}, pages={4752–4761} }
 @article{joshi_vahlenkamp_garg_tompkins_tompkins_2004, title={Preferential replication of FIV in activated CD4(+)CD25(+)T cells independent of cellular proliferation}, volume={321}, ISSN={["0042-6822"]}, DOI={10.1016/j.virol.2004.01.014}, abstractNote={Studies attempting to identify reservoirs of HIV-1 latency have documented that the virus persists as both a latent and productive infection in subsets of CD4+ cells. Reports regarding establishment of a stable HIV-1 infection in quiescent T cells in vitro, however, are controversial. In the present study, we investigated the susceptibility of naive and activated CD4+ cell subsets (distinguished by differential expression of CD25) to feline immunodeficiency virus (FIV) infection, their ability to replicate the virus, and potentially act as a reservoir for virus persistence in infected animals. While both CD4+CD25+ and CD4+CD25− cells are susceptible to FIV infection in vitro and in vivo, only CD4+CD25+ cells produce infectious virions when cultured with interleukin-2 (IL-2). Latently infected CD4+CD25− cells produce infectious virions following ConcanvalinA (ConA) stimulation, which correlates with upregulated surface expression of CD25. In contrast to CD4+CD25− cells, CD4+CD25+ cells remain unresponsive to mitogen stimulation and are relatively resistant to apoptosis whether or not infected with FIV. The ability of CD4+CD25+ cells to replicate FIV efficiently in the presence of IL-2 but remain anergic and unresponsive to apoptotic signaling suggests that these cells may provide a reservoir of productive FIV infection. On the contrary, CD4+CD25− cells seem to establish as latent viral reservoirs capable of being reactivated after stimulation.}, number={2}, journal={VIROLOGY}, author={Joshi, A and Vahlenkamp, TW and Garg, H and Tompkins, WAF and Tompkins, MB}, year={2004}, month={Apr}, pages={307–322} }
 @article{bull_vahlenkamp_dow_collisson_winslow_phadke_tompkins_tompkins_2004, title={Spontaneous T cell apoptosis in feline immunodeficiency virus (FIV)-infected cats is inhibited by IL2 and anti-B7.1 antibodies}, volume={99}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2004.01.010}, abstractNote={Lymph node (LN) T cells from feline immunodeficiency virus (FIV)-infected cats have an increased expression of B7 co-stimulatory molecules as well as their ligand CTLA4, resembling an activation phenotype shown to induce anergy and apoptosis in activated T cells. In addition, LN T cells from FIV-infected cats also show increased spontaneous apoptosis compared to uninfected animals. The apoptosis observed in these animals occurs primarily in T cells expressing B7 and CTLA4, suggesting a role for B7 and CTLA4 interactions in the induction of anergy/apoptosis. In order to investigate the role of B7 and CTLA4 interactions on T cell apoptosis in LN T cells from FIV-infected cats, we performed blocking experiments by measuring T cell apoptosis in LN T cell cultures treated with anti-feline B7.1, B7.2, and CTLA4 specific antibodies, as well as interleukin (IL)-2. The addition of IL2, the primary cytokine produced by B7/CD28 interactions, resulted in a significant decrease of T cell apoptosis in cultured LN cells as assessed by two-color flow cytometry and TUNEL assay. The addition of anti-B7.1 antibodies significantly inhibited T cell apoptosis in FIV-infected cats with low-level plasma viremia, while addition of anti-B7.2 and anti-CTLA4 antibodies had no affect. These results suggest a role of B7 signaling in the increased spontaneous apoptosis observed in LN T cells from FIV-infected animals.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Bull, ME and Vahlenkamp, TW and Dow, JL and Collisson, EW and Winslow, BJ and Phadke, AP and Tompkins, MB and Tompkins, WAF}, year={2004}, month={May}, pages={25–37} }
 @article{langbein_kuhnlein_schimmer_vahlenkamp_huebner_muller_2003, title={Generation of reference values for the characterization of lymphocyte subpopulations in the peripheral blood of dogs and cats}, volume={48}, number={9}, journal={Kleintier-Praxis}, author={Langbein, I. and Kuhnlein, P. and Schimmer, C. and Vahlenkamp, T. W. and Huebner, J. and Muller, E.}, year={2003}, pages={537-} }
 @article{hudson_vahlenkamp_howard_colby_tompkins_meeker_2002, title={Cerebrospinal fluid centesis at the cerebellomedullary cistern of kittens}, volume={41}, number={5}, journal={Contemporary Topics in Laboratory Animal Science}, author={Hudson, L. C. and Vahlenkamp, T. W. and Howard, K. E. and Colby, B. and Tompkins, M. B. and Meeker, R. B.}, year={2002}, pages={30–32} }
 @article{tompkins_bull_dow_ball_collisson_winslow_phadke_vahlenkamp_tompkins_2002, title={Feline immunodeficiency virus infection is characterized by B7(+)CTLA4(+) T cell apoptosis}, volume={185}, ISSN={["0022-1899"]}, DOI={10.1086/339847}, abstractNote={The B7.1 and B7.2 costimulatory molecules on antigen-presenting cells provide second signals for regulating T cell immune responses via CD28 and cytotoxic T lymphocyte antigen 4 (CTLA4) on T cells. CD28 signals cell proliferation, whereas CTLA4 signals for anergy or apoptosis, terminating the immune response. Because T cell apoptosis and immunodeficiency is a characteristic of feline immunodeficiency virus (FIV)-infected cats, it is possible that negative T cell signaling via B7 and CTLA4 may be favored in these cats. Flow cytometry revealed high percentages of CD8+ and CD4+ cells expressing B7.1, B7.2, and CTLA4 in lymph nodes of FIV-positive cats and a large fraction of CTLA4+ T cells coexpressing B7.1 and B7.2. Three-color analysis with anti-B7.1, anti-B7.2, or anti-CTLA4 and TUNEL (terminal deoxynucleotidyl transferase nick-end-labeling) analysis revealed that apoptosis was a characteristic of B7.1+ B7.2+ CTLA4+ T cells. These data support the hypothesis that lymph node apoptosis and immune deterioration in FIV-infected cats results from chronic B7.1- and/or B7.2-CTLA4-mediated T-T interactions.}, number={8}, journal={JOURNAL OF INFECTIOUS DISEASES}, author={Tompkins, MB and Bull, ME and Dow, JL and Ball, JM and Collisson, EW and Winslow, BJ and Phadke, AP and Vahlenkamp, TW and Tompkins, WA}, year={2002}, month={Apr}, pages={1077–1093} }
 @article{vahlenkamp_konrath_weber_muller_2002, title={Persistence of Borna disease virus in naturally infected sheep}, volume={76}, ISSN={["0022-538X"]}, DOI={10.1128/JVI.76.19.9735-9743.2002}, abstractNote={ABSTRACT}, number={19}, journal={JOURNAL OF VIROLOGY}, author={Vahlenkamp, TW and Konrath, A and Weber, M and Muller, H}, year={2002}, month={Oct}, pages={9735–9743} }
 @inproceedings{vahlenkamp_bull_dow_anderson_tompkins_tompkins_2001, title={B7.1/B7.2 and CTLA4 expression on feline T cells in vitro correlates with apoptosis}, number={2001}, booktitle={Journal of Leukocyte Biology}, author={Vahlenkamp, T. W. and Bull, M. E. and Dow, J. and Anderson, J. and Tompkins, M. B. and Tompkins, W. A. F.}, year={2001}, pages={255} }
 @article{kacza_mohr_pannicke_kuhrt_dietzel_fluss_richt_vahlenkamp_stahl_reichenbach_et al._2001, title={Changes of the organotypic retinal organization in Borna virus-infected Lewis rats}, volume={30}, ISSN={["0300-4864"]}, DOI={10.1023/A:1019641404940}, abstractNote={Retinae of Borna disease virus (BDV)-infected Lewis rats were investigated with emphasis on long-term changes in organotypic tissue organization and glia-neuron relationship. Virus inoculation was attained via intracerebral BDV injection. Following survival times ranging between two and eight months, the retinal thickness was reduced up to one third of that of controls. Photoreceptor segments were completely extinguished and the number of neurons was dramatically reduced. The typical laminar organization of the retina was largely dissolved. Electron microscopy revealed severe spongy degeneration. Large numbers of activated microglia and macrophages were found, both cell types performing very active phagocytosis. The microglial cells expressed an extraordinary phenotype as characterized by large numbers of processes, with some of them penetrating the endfeet of Müller cells and others establishing highly complex interdigitations with vacuolized swellings and endings of neuronal processes. Müller cells were not reduced in number but displayed clear indications of gliosis such as alterations in the immunoreactivity for filament proteins and glutamine synthetase, significantly thickened stem processes, and an altered pattern of K(+) currents in patch-clamp recordings. These findings demonstrate for the first time long-term neuron-glia interactions in the retina of BDV-infected rats. Moreover, the data contribute to our knowledge on structural and functional alterations accompanying persisting virus infection in the central nervous system.}, number={9-10}, journal={JOURNAL OF NEUROCYTOLOGY}, author={Kacza, J and Mohr, C and Pannicke, T and Kuhrt, H and Dietzel, J and Fluss, M and Richt, JA and Vahlenkamp, TW and Stahl, T and Reichenbach, A and et al.}, year={2001}, pages={801–820} }
 @inproceedings{bull_vahlenkamp_tompkins_tompkins_2001, title={T cell apoptosis in FIV-infected cats is blocked by the addition of antibodies to B7.1 and B7.2}, number={2001}, booktitle={Journal of Leukocyte Biology}, author={Bull, M. E. and Vahlenkamp, T. W. and Tompkins, M. B. and Tompkins, W. A. F.}, year={2001}, pages={256} }