PMID- 6268886
OWN - NLM
STAT- MEDLINE
DCOM- 19811122
LR  - 20081121
IS  - 0027-8874 (Print)
IS  - 0027-8874 (Linking)
VI  - 67
IP  - 4
DP  - 1981 Oct
TI  - Determinants of susceptibility and resistance to feline leukemia virus infection. 
      II. Susceptibility of feline lymphocytes to productive feline leukemia virus 
      infection.
PG  - 899-910
AB  - The interplay between feline leukemia virus (FeLV) and feline lymphocytes (lc) 
      infected in vitro or in vivo was investigated. Surface marker analysis and viral 
      infectivity (VI) assays of lc populations were used to determine susceptibility 
      of lc subsets to FeLV. The principal FeLV-replicating cell in the mesenteric 
      lymph node of persistently infected, preleukemic cats was a nonadherent, 
      complement receptor (CR)-bearing lc (B-cell). The lymph nodes of preleukemic cats 
      also had increased numbers of uninfected T-cells [cells forming rosettes with 
      guinea pig erythrocytes (GPE)] and cells with receptors for the Fc portion of 7S 
      IgG (Fc gamma R cells) as compared with lymph nodes of age-matched 
      specific-pathogen-free (SPF) cats. The induction of productive infection of 
      feline peripheral blood mononuclear leukocytes (PBL) in vitro depended on a 
      48-hour in vitro preincubation period before virus exposure. The equivalent 
      susceptibility of whole and adherent cell-depleted PBL to productive infection 
      and the failure of hydrocortisone to enhance viral infection were compatible with 
      identification of the FeLV-replicating cell as an lc. Furthermore, lc from 
      susceptible SPF kittens replicated 50 times as much FeLV as did lc from resistant 
      adult SPF cats. The Ic productively infected with FeLV after in vitro exposure 
      were more precisely identified with the use of Ficoll-Isopaque density gradient 
      separations of rosetted and nonrosetted lc. Whole PBL, GPE rosette-positive PBL 
      (T-cells), and CR-positive PBL (B-cells) were permissive to FeLV infection, and 
      maximal VI was evident at 14 days after exposure. The substantial (1,325-fold) 
      increment in VI found in the Fc gamma R-depleted PBL suggested a role for Fc 
      gamma R cells in the containment of FeLV infection. Unstimulated mononuclear 
      leukocytes from blood, spleen, lymph node, thymus, and marrow were susceptible to 
      productive FeLV infection after in vitro exposure. The degree of spontaneous DNA 
      synthesis in marrow, thymus, and spleen but not lymph node or PBL was inversely 
      related to permissiveness to viral replication. Mitogen activation of lc was 
      associated with decreased viral replication when either T-cell mitogens 
      (concanavalin A, phytohemagglutinin, or pokeweed mitogen) or a B-cell mitogen 
      (dextran sulfate) was used. Virus production by spleen cells and PBL was enhanced 
      twofold to tenfold by prior lc stimulation by the B-cell mitogen, 
      lipopolysaccharide, or protein A-bearing Staphylococcus aureus, a mitogen for 
      feline T-cells with Fc gamma R. Both productively infected (preincubated) and 
      nonproductively infected (freshly isolated) PBL transferred infectious FeLV to 
      autochthonous peritoneal macrophages (M theta); most of the virus in 
      PBL-peritoneal M theta cocultures was produced by adherent cells, irrespective of 
      whether the adherent or nonadherent cell population was inoculated originally.
FAU - Rojko, J L
AU  - Rojko JL
FAU - Hoover, E A
AU  - Hoover EA
FAU - Finn, B L
AU  - Finn BL
FAU - Olsen, R G
AU  - Olsen RG
LA  - eng
GR  - 1-F32-CA06087-03/CA/NCI NIH HHS/United States
GR  - N01-CP91008-05/CP/NCI NIH HHS/United States
GR  - R01-CA22527-03/CA/NCI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Natl Cancer Inst
JT  - Journal of the National Cancer Institute
JID - 7503089
RN  - 0 (Mitogens)
SB  - IM
MH  - Age Factors
MH  - Animals
MH  - Cats
MH  - Immunity, Innate
MH  - Leukemia Virus, Feline/immunology
MH  - Leukemia, Experimental/*immunology/microbiology
MH  - Lymphocyte Activation
MH  - Lymphocytes/*immunology/microbiology
MH  - Macrophages/microbiology
MH  - Mitogens/pharmacology
MH  - Virus Replication
EDAT- 1981/10/01 00:00
MHDA- 1981/10/01 00:01
CRDT- 1981/10/01 00:00
PHST- 1981/10/01 00:00 [pubmed]
PHST- 1981/10/01 00:01 [medline]
PHST- 1981/10/01 00:00 [entrez]
PST - ppublish
SO  - J Natl Cancer Inst. 1981 Oct;67(4):899-910.