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Influenza A virus interaction with murine lymphocytes. I. The influence of influenza virus A/Japan 305 (H2N2) on the pattern of migration of recirculating lymphocytes.

Identifieur interne : 001152 ( Ncbi/Checkpoint ); précédent : 001151; suivant : 001153

Influenza A virus interaction with murine lymphocytes. I. The influence of influenza virus A/Japan 305 (H2N2) on the pattern of migration of recirculating lymphocytes.

Auteurs : J J Woodruff ; J F Woodruff

Source :

RBID : pubmed:60451

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English descriptors

Abstract

The effect of influenza virus A/Japan 305 (H2N2) on the path of migration of recirculating lymphocytes has been studied. 51Cr-labeled rat thoracic duct lymphocytes (TDL) were incubated with virus at 37 degrees C for 1 hr and then infused i.v. into syngeneic recipients which were killed 1 hr later. Virus-treated TDL accumulated in the liver and their recovery in lymph nodes and spleen was severely reduced. Changes in lymphocytes induced by virus developed rapidly and were evident after incubation for only 15 min. UV-irradiated virus altered the pattern of lymphocyte localization but attachment of heat-inactivated virus to lymphocytes in vitro had no effect on their distribution in vivo. Evidence was obtained that some virus-treated TDL, initially sequestered in the liver, subsequently recovered their ability to circulate normally. Recovery was not complete and a population of cells failed to regain their ability to home into lymph nodes. Evidence is also presented demonstrating that influenza virus affected the homing properties of both T and B cells. It is suggested that aberrations in lymphocyte homing were mediated by the viral neuraminidase which induces changes in the cell membrane leading to their accumulation in the liver.

PubMed: 60451


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pubmed:60451

Le document en format XML

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<term>Influenza A virus (enzymology)</term>
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<term>Liver (cytology)</term>
<term>Lung (cytology)</term>
<term>Lymph Nodes (cytology)</term>
<term>Lymphocytes (immunology)</term>
<term>Neuraminidase (metabolism)</term>
<term>Orthomyxoviridae (immunology)</term>
<term>Radiation Effects</term>
<term>Rats</term>
<term>Rats, Inbred Strains</term>
<term>Receptors, Drug</term>
<term>Spleen (cytology)</term>
<term>Surface Properties</term>
<term>T-Lymphocytes (immunology)</term>
<term>Temperature</term>
<term>Time Factors</term>
<term>Ultraviolet Rays</term>
<term>Virus Replication</term>
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<term>Alphafoetoprotéines (pharmacologie)</term>
<term>Animaux</term>
<term>Effets des rayonnements</term>
<term>Facteurs temps</term>
<term>Foie (cytologie)</term>
<term>Lignées consanguines de rats</term>
<term>Lymphocytes (immunologie)</term>
<term>Lymphocytes B (immunologie)</term>
<term>Lymphocytes T (immunologie)</term>
<term>Mouvement cellulaire ()</term>
<term>Noeuds lymphatiques (cytologie)</term>
<term>Orthomyxoviridae (immunologie)</term>
<term>Poumon (cytologie)</term>
<term>Propriétés de surface</term>
<term>Rate (cytologie)</term>
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<term>Rayons ultraviolets</term>
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<term>Réplication virale</term>
<term>Sialidase (métabolisme)</term>
<term>Sous-type H2N2 du virus de la grippe A</term>
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<term>Mouvement cellulaire</term>
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<term>Rayons ultraviolets</term>
<term>Récepteurs des médicaments</term>
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<div type="abstract" xml:lang="en">The effect of influenza virus A/Japan 305 (H2N2) on the path of migration of recirculating lymphocytes has been studied. 51Cr-labeled rat thoracic duct lymphocytes (TDL) were incubated with virus at 37 degrees C for 1 hr and then infused i.v. into syngeneic recipients which were killed 1 hr later. Virus-treated TDL accumulated in the liver and their recovery in lymph nodes and spleen was severely reduced. Changes in lymphocytes induced by virus developed rapidly and were evident after incubation for only 15 min. UV-irradiated virus altered the pattern of lymphocyte localization but attachment of heat-inactivated virus to lymphocytes in vitro had no effect on their distribution in vivo. Evidence was obtained that some virus-treated TDL, initially sequestered in the liver, subsequently recovered their ability to circulate normally. Recovery was not complete and a population of cells failed to regain their ability to home into lymph nodes. Evidence is also presented demonstrating that influenza virus affected the homing properties of both T and B cells. It is suggested that aberrations in lymphocyte homing were mediated by the viral neuraminidase which induces changes in the cell membrane leading to their accumulation in the liver.</div>
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