InforLorV4, Istex, Corpus, bibRecord, 002D44

Pathogenesis of Experimental Feline Leukemia Virus Infection

Identifieur interne : 002D44 ( Istex/Corpus ); précédent : 002D43; suivant : 002D45

Pathogenesis of Experimental Feline Leukemia Virus Infection

Auteurs : Jennifer L. Rojko ; Edward A. Hoover ; Lawrence E. Mathes ; Richard G. Olsen ; Joseph P. Schaller

Source :

Journal of the National Cancer Institute [ 0027-8874 ] ; 1979-09.

RBID : ISTEX:BF4392F0842CEDDBB72DAE631A6F84F65AB65F9C

Abstract

Early events in the pathogenesis of feline leukemia virus (FeLV) infection were studied in 59 specific-pathogen-free cats. Young cats (≤8 wk old and highly susceptible to FeLV) and adult cats (>6 mo old and relatively resistant to FeLV) were exposed to FeLV by oral-nasal, ip, or sc inoculation. The sequential distribution of FeLV group-specific antigen (GSA) in blood and tissues of susceptible versus resistant cats was correlated with alterations in hematologic and serologic parameters. Six sequential phases of FeLV infection (i.e., viral replication) were identified: 1) lymphoreticular cells in local lymphoid tissues [2–14 days after exposure (DAE)]; 2) circulating lymphocytes and monocytes (early cell-associated viremia) (1–14 DAE); 3) lymphoid germinal cells in lymphoid tissues throughout the body (3–12 DAE); 4) bone marrow neutrophil and platelet precursor cells and intestinal crypt epithelium (7–21 DAE); 5) circulating neutrophils and platelets (with establishment of viremia) (≥14–28 DAE); and 6) mucosal and glandular epithelial tissues (with excretion of FeLV) (≥28–56 DAE). Early lymphoreticular virus replication (phases 1–3) was present in both progressive and transient infection. In cats that became persistently infected (80% of young cats and 14% of adult cats), FeLV infection was not contained in the initial lymphoreticular phases 1–3, and extensive virus replication occurred in the germinal cell populations of lymphoid, hematopoietic, and epithelial tissues (phases 3–6). In cats with progressive infections, lymphopenia and neutropenia (21–56 DAE) were associated with the appearance of FeLV GSA in circulating neutrophils and platelets (≥14–28 DAE). In cats with self-limiting infections, virus containment in phases 3 or 4 correlated with transient lymphopenia (7–14 DAE) and development of antibody to the feline oncornavirus-associated cell membrane antigen.

Url:

https://api.istex.fr/ark:/67375/HXZ-337NSJ8F-8/fulltext.pdf

DOI: 10.1093/jnci/63.3.759

Links to Exploration step

ISTEX:BF4392F0842CEDDBB72DAE631A6F84F65AB65F9C

Le document en format XML

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<front><div type="abstract">Early events in the pathogenesis of feline leukemia virus (FeLV) infection were studied in 59 specific-pathogen-free cats. Young cats (≤8 wk old and highly susceptible to FeLV) and adult cats (>6 mo old and relatively resistant to FeLV) were exposed to FeLV by oral-nasal, ip, or sc inoculation. The sequential distribution of FeLV group-specific antigen (GSA) in blood and tissues of susceptible versus resistant cats was correlated with alterations in hematologic and serologic parameters. Six sequential phases of FeLV infection (i.e., viral replication) were identified: 1) lymphoreticular cells in local lymphoid tissues [2–14 days after exposure (DAE)]; 2) circulating lymphocytes and monocytes (early cell-associated viremia) (1–14 DAE); 3) lymphoid germinal cells in lymphoid tissues throughout the body (3–12 DAE); 4) bone marrow neutrophil and platelet precursor cells and intestinal crypt epithelium (7–21 DAE); 5) circulating neutrophils and platelets (with establishment of viremia) (≥14–28 DAE); and 6) mucosal and glandular epithelial tissues (with excretion of FeLV) (≥28–56 DAE). Early lymphoreticular virus replication (phases 1–3) was present in both progressive and transient infection. In cats that became persistently infected (80% of young cats and 14% of adult cats), FeLV infection was not contained in the initial lymphoreticular phases 1–3, and extensive virus replication occurred in the germinal cell populations of lymphoid, hematopoietic, and epithelial tissues (phases 3–6). In cats with progressive infections, lymphopenia and neutropenia (21–56 DAE) were associated with the appearance of FeLV GSA in circulating neutrophils and platelets (≥14–28 DAE). In cats with self-limiting infections, virus containment in phases 3 or 4 correlated with transient lymphopenia (7–14 DAE) and development of antibody to the feline oncornavirus-associated cell membrane antigen.</div>
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<p>Supported by Public Health Service (PHS) grant R01-CA22527-01 from the National Cancer Institute (NCI); by PHS fellowship 1-F32-CA06087-01 from the NCI; by PHS contract N01-1-CP53572 from the Division of Cancer Cause and Prevention, NCI; and by PHS contract N01-1-CB74159 from the Division of Cancer Biology and Diagnosis, NCI.</p>
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<name><surname>Rojko</surname>
<given-names>Jennifer L.</given-names>
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<name><surname>Hoover</surname>
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<name><surname>Mathes</surname>
<given-names>Lawrence E.</given-names>
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<name><surname>Olsen</surname>
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<name><surname>Schaller</surname>
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<xref ref-type="aff" rid="au3">3</xref>
<xref ref-type="fn" rid="FN5">5</xref>

</contrib>

<aff id="au3"><label>3</label>
<institution>Department of Veterinary Pathobiology, The Ohio State University</institution>
, <addr-line>1925 Coffey Rd., Columbus, Ohio 43210</addr-line>
.</aff>

<aff id="au4"><label>4</label>
<institution>The Ohio State University Comprehensive Cancer Center</institution>
, <addr-line>357 McCampbell Hall, 1580 Cannon Drive, Columbus, Ohio 43210</addr-line>
.</aff>

</contrib-group>

<author-notes>

<fn id="FN5" fn-type="other"><label>5</label>
<p>We acknowledge the excellent assistance provided by Mr. Kenneth Milliser, Ms. Pamela Wilson, Mr. Patrick Adams, and Ms. Nancy Mesoloras.</p>
</fn>

</author-notes>

<pub-date pub-type="ppub">

<month>9</month>

<year>1979</year>

</pub-date>

<volume>63</volume>

<issue>3</issue>

<fpage>759</fpage>

<lpage>768</lpage>

<history>

<date date-type="received">

<day>27</day>

<month>10</month>

<year>1978</year>

</date>

<date date-type="accepted">

<day>11</day>

<month>3</month>

<year>1979</year>

</date>

</history>

<copyright-year>1979</copyright-year>

<abstract>

<title>Abstract</title>

<p>Early events in the pathogenesis of feline leukemia virus (FeLV) infection were studied in 59 specific-pathogen-free cats. Young cats (≤8 wk old and highly susceptible to FeLV) and adult cats (>6 mo old and relatively resistant to FeLV) were exposed to FeLV by oral-nasal, ip, or sc inoculation. The sequential distribution of FeLV group-specific antigen (GSA) in blood and tissues of susceptible versus resistant cats was correlated with alterations in hematologic and serologic parameters. Six sequential phases of FeLV infection (i.e., viral replication) were identified: 1) lymphoreticular cells in local lymphoid tissues [2–14 days after exposure (DAE)]; 2) circulating lymphocytes and monocytes (early cell-associated viremia) (1–14 DAE); 3) lymphoid germinal cells in lymphoid tissues throughout the body (3–12 DAE); 4) bone marrow neutrophil and platelet precursor cells and intestinal crypt epithelium (7–21 DAE); 5) circulating neutrophils and platelets (with establishment of viremia) (≥14–28 DAE); and 6) mucosal and glandular epithelial tissues (with excretion of FeLV) (≥28–56 DAE). Early lymphoreticular virus replication (phases 1–3) was present in both progressive and transient infection. In cats that became persistently infected (80% of young cats and 14% of adult cats), FeLV infection was not contained in the initial lymphoreticular phases 1–3, and extensive virus replication occurred in the germinal cell populations of lymphoid, hematopoietic, and epithelial tissues (phases 3–6). In cats with progressive infections, lymphopenia and neutropenia (21–56 DAE) were associated with the appearance of FeLV GSA in circulating neutrophils and platelets (≥14–28 DAE). In cats with self-limiting infections, virus containment in phases 3 or 4 correlated with transient lymphopenia (7–14 DAE) and development of antibody to the feline oncornavirus-associated cell membrane antigen.</p>

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</titleInfo>
<name type="personal"><namePart type="given">Jennifer L.</namePart>
<namePart type="family">Rojko</namePart>
<affiliation>Department of Veterinary Pathobiology, The Ohio State University, 1925 Coffey Rd., Columbus, Ohio 43210.</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Edward A.</namePart>
<namePart type="family">Hoover</namePart>
<affiliation>Department of Veterinary Pathobiology, The Ohio State University, 1925 Coffey Rd., Columbus, Ohio 43210.</affiliation>
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<name type="personal"><namePart type="given">Lawrence E.</namePart>
<namePart type="family">Mathes</namePart>
<affiliation>Department of Veterinary Pathobiology, The Ohio State University, 1925 Coffey Rd., Columbus, Ohio 43210.</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Richard G.</namePart>
<namePart type="family">Olsen</namePart>
<affiliation>Department of Veterinary Pathobiology, The Ohio State University, 1925 Coffey Rd., Columbus, Ohio 43210.</affiliation>
<affiliation>The Ohio State University Comprehensive Cancer Center, 357 McCampbell Hall, 1580 Cannon Drive, Columbus, Ohio 43210.</affiliation>
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<name type="personal"><namePart type="given">Joseph P.</namePart>
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<description>5We acknowledge the excellent assistance provided by Mr. Kenneth Milliser, Ms. Pamela Wilson, Mr. Patrick Adams, and Ms. Nancy Mesoloras.</description>
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Pathogenesis of Experimental Feline Leukemia Virus Infection

Pathogenesis of Experimental Feline Leukemia Virus Infection

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