Participation of Lymphocytes in Viral Infections

Ef, Wheelock; St, Toy

doi:10.1016/s0065-2776(08)60297-7

Cited by 116 publications

(55 citation statements)

References 274 publications

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“…First indications that cell activation played a role in viral replication began to emerge at about the same early time, however. Thus, viruses were shown to grow better in lymphocytes treated with mitogenic lectins (7,8) and influenza viruses of the H2N2 subtype were found to activate lymphocytes mitogenically (9). In a study on the biochemical effects of Semliki Forest virus on chicken embryo cells, we noted that the alterations induced in mitochondria by this Togavirus were similar to those induced by treatment with fetal calf serum, a well-known mitogenic stimulus (10).…”

Section: Introductionmentioning

confidence: 92%

Reactive oxygen species and nitric oxide in viral diseases

Peterhans

1997

Biol Trace Elem Res

118

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Metabolites derived from superoxide (02"-) and nitric oxide (NO.) play an important role in antimicrobial and antitumoral defense, but may also harm the host. Low levels of such metabolites can also facilitate viral replication because of their mitogenic effects on cells. Most viruses grow better in proliferating cells, and indeed, many viruses induce in their host cell changes similar to those seen early after treatment with mitogenic lectins. Influenza and paramyxoviruses activate in phagocytes the generation of superoxide by a mechanism involving the interaction between the viral surface glycoproteins and the phagocyte's plasma membrane. Interestingly, viruses that activate this host defense mechanism are toxic when injected in the bloodstream of animals. Mice infected with influenza virus undergo oxidative stress. In addition, a wide array of cytokines are formed in the lung, contributing to the systemic effects of influenza. Oxidative stress is seen also in chronic viral infections, such as AIDS and viral hepatitis. Oxidant production in viral hepatitis may contribute to the emergence of hepatocellular carcinoma, a tumor seen in patients after years of chronic inflammation of the liver. Antioxidants and agents that downregulate proinflammatory cytokines and lipid mediators may be a useful complement to specific antiviral drugs in the therapy of viral diseases.

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Section: Introductionmentioning

confidence: 92%

Reactive oxygen species and nitric oxide in viral diseases

Peterhans

1997

Biol Trace Elem Res

118

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“…VIR ~0 1973;Olding et al 1975), while other viruses, such as measles virus (Joseph et al 1975) and herpes simplex virus (Rinaldo et al I978) have been shown to replicate in both cell types when activated with a suitable mitogen. Although rescue of virus from the population normally non-permissive to virus replication has not previously been reported, Bloom et al (I976) found that uptake of VSV into both T and B cells did occur, and by studying the infection of B lymphoblastoid cell lines they found that I3S and 26S mRNA species were synthesized and that the point of restriction appeared to be the synthesis of 42S virion RNA.…”

Section: I2mentioning

confidence: 99%

Replication and Expression of Rubella Virus in Human Lymphocyte Populations

Chantler¹,

Tingle²

1980

Journal of General Virology

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~UMMARYHuman mononuclear cells (lymphocytes and monocytes) from peripheral blood were examined for their ability to support the replication of rubella virus (RV) after infection in vitro. Replication was shown to occur in mixed lymphocytes and to be enhanced by stimulation with phytohaemagglutinin or pokeweed mitogen. A comparison of RV polypeptide synthesis in lymphocytes and RKr 3 cells showed no major differences in the polypeptides induced by infection. However, cellular translation was inhibited in the lymphocytes facilitating identification of virus polypeptides and eliminating the need for hypertonic labelling conditions used with RKI3 cells. RV replication was also shown to occur in sub-populations of T-cells but not in B-cells. However, RV could be rescued from the B and monocyte population by co-cultivation with RKI3 cells.

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“…These relationships and interactions are complicated by the reported suppressive effects of viruses on lymphocyte function (13,14) as well as of viral infection on the immune response (15).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms responsible for defective human T-lymphocyte sheep erythrocyte rosette function associated with hepatitis B virus infections.

Chisari¹,

Routenberg²,

Edgington³

1976

J. Clin. Invest.

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A B S T R A C T The expression of selected lymphocyte surface-membrane markers was evaluated in 37 patients with acute viral hepatitis B, 10 of whom were studied serially through the resolving and convalescent phases of disease. Bone marrow-derived (B) lymphocytes were identified by reference to surface immunoglobulin, whereas normal thymus-derived (T) lymphocytes were assayed by their capacity to form spontaneous nonim- Both intrinsic and extrinsic suppression of T lymphocyte ER function commonly occurred during the first 4 wk of acute viral hepatitis B. 9 of the 10 patients followed serially continued to manifest defective ER function at 12 wk. However, the intrinsic defect was observable only in those patients whose liver disease had resolved or was resolving, whereas the extrinsic defect was observed only in two patients with biochemical and histological evidence of unresolved hepatitis at that time.

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Participation of Lymphocytes in Viral Infections

Cited by 116 publications

References 274 publications

Reactive oxygen species and nitric oxide in viral diseases

Reactive oxygen species and nitric oxide in viral diseases

Replication and Expression of Rubella Virus in Human Lymphocyte Populations

Mechanisms responsible for defective human T-lymphocyte sheep erythrocyte rosette function associated with hepatitis B virus infections.

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