BRIEF REPORT The distribution of feline immunodeficiency virus in tissue compartments of feral domestic cats Jessica J. Hayward • Allen G. Rodrigo Received: 2 October 2009 / Accepted: 21 December 2009 / Published online: 29 January 2010 Ó Springer-Verlag 2010 Prevalence and subtype studies of feline immunodeficiency virus (FIV) in the domestic cat (Felis catus) have been conducted thoroughly. However, the intrahost dynamics of FIV have been less well studied. Here, we determine the diversity of FIV env V3–V6 sequences isolated from multiple tissues of naturally infected feral cats. Using nested PCR, FIV was amplified from non-lymphoid tissues from eight of sixteen cats that had amplifiable proviral FIV DNA in the popliteal lymph node. In general, we found low intrahost FIV diversity, but there was evidence of tissue compartmentalization in one cat. Feline immunodeficiency virus is a lentivirus, closely related to human immunodeficiency virus (HIV), which can cause immunodeficiency in F. catus [17]. FIV has been detected in a number of tissue types, including lymphoid tissue, central nervous system (CNS), bone marrow, intestine, liver and lung [2, 4, 15, 22]. Compartmentalization is the restriction of virus move- ment between different tissues or cell types [14]. Studies on HIV-1 have shown compartmentalization in the genitouri- nary tract, CNS and lung when compared to peripheral blood in the same individuals [1, 10–12]. Two recent studies have shown FIV compartmentalization in the CNS soon after experimental infection [9, 13]. To date, there has been no demonstration of an extensive restriction of movement of FIV and no evidence involving natural FIV infections. Here, the diversity of FIV in different tissues of natu- rally infected feral cats is investigated, with the aim to look for evidence of compartmentalization. Combinations of seven tissues (lymph node, tongue, liver, lung, kidney, testis, brain stem) were dissected from sixteen cats trapped at two New Zealand (NZ) locations in 2004–2005. Geno- mic DNA was extracted and the env V3–V6 region was amplified as described previously [7]. PCR products were directly sequenced to confirm the presence of FIV in each tissue. Although all sixteen cats sampled in this study were FIV-positive by PCR from lymph node, we were able to amplify FIV from at least one other tissue from eight cats only (Table 1). The group of eight cats from which non- lymphoid tissues yielded FIV had a significantly higher mean lymph node proviral load than those cats that lacked FIV in non-lymphoid tissue (Student’s t = 2.72, p \ 0.05, df = 14). A previous HIV-1 study found a clear correlation between high proviral load in non-lymphoid tissues and advanced stage of infection [5]. These results could explain the inability to amplify FIV from many of the tissues sampled in the present study, that is, the cats from which non-lymphoid FIV was not found might be in the early stages of FIV infection. This has been documented for HIV-1, where the virus is found in high numbers in lym- phoid tissue during clinical latency and, as disease pro- gresses, spills over into the blood and invades other tissues [16, 30]. It is also possible that FIV is present in the tissues, but at a level below the detection limits of this study, or in other parts of sampled tissue [5]. Endpoint dilution sequencing was used to obtain a target of ten sequences per tissue [7, 21]. All FIV sequences J. J. Hayward Á A. G. Rodrigo Bioinformatics Institute, Allan Wilson Centre for Molecular Ecology and Evolution, School of Biological Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand Present Address: J. J. Hayward (&) Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Hungerford Hill Road, Ithaca, NY 14853, USA e-mail: jjh276@cornell.edu 123 Arch Virol (2010) 155:411–416 DOI 10.1007/s00705-010-0598-z