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PubMed2005

Viruses and autoimmunity.

Viruses have been suspected as causes and contributors of human autoimmune diseases (AID), although direct evidence for the association is lacking. However, several animal models provide strong evidence that viruses can induce AIDs as well as act to accelerate and exacerbate lesions in situations where self-tolerance is broken. Many models support the hypothesis by acting as molecular mimics that stimulate self-reactive lymphocytes. Mimicry alone is usually inadequate and with human AID, no compelling evidence supports a role for viruses that are acting as molecular mimics. Alternative mechanisms by which viruses participate in autoimmunity are non-specific, involving a mechanistically poorly understood process termed bystander activation or perhaps viral interference with regulatory cell control systems. This review briefly discusses examples where viruses are involved, taking the viewpoint that molecular mimicry is over emphasized as a critical mechanism during AID pathogenesis.

Animals↗
PubMed2006

Viruses and autoimmunity.

Viruses have been suspected as causes and contributors of human autoimmune diseases (AID), although direct evidence for the association is lacking. However, several animal models provide strong evidence that viruses can induce AIDs as well as act to accelerate and exacerbate lesions in situations where self-tolerance is broken. Many models support the hypothesis by acting as molecular mimics that stimulate self-reactive lymphocytes. Mimicry alone is usually inadequate and with human AID, no compelling evidence supports a role for viruses that are acting as molecular mimics. Alternative mechanisms by which viruses participate in autoimmunity are non-specific, involving a mechanistically poorly understood process termed bystander activation or perhaps viral interference with regulatory cell control systems. This review briefly discusses examples where viruses are involved, taking the view point that molecular mimicry is over emphasized as a critical mechanism during AID pathogenesis.

Animals↗
PubMed1985

Blocked coated pits in AtT20 cells result from endocytosis of budding retrovirions.

AtT20 cells support the replication of two endogenous retroviruses, a murine leukemia virus and a mouse mammary tumor virus. On glass or plastic substrates, AtT20 cells grow in clumps. In this situation, retroviruses budding from the plasma membrane of one cell can, on rare occasions, be invested by coated pits in the plasma membranes of contiguous cells. These pits can invaginate to depths of 2,000-4,000 A within the cytoplasm drawing with them the viral buds which remain connected to their parental cells by tubular stalks, some of which are only 225 +/- 15 A in diameter. These stalks run down the straight necks of the pits from the buds to the parental cell surfaces. Several lines of evidence indicate that these unique structures are blocked such that neither endocytosis nor budding can go to completion, and that they persist for several hours. The properties of these blocked coated pits are relevant to models of both endocytosis and viral budding. First, they indicate that the invagination of a coated pit is not absolutely dependent on its pinching off to form a coated vesicle, but that uncoating appears to be dependent upon the generation of a free vesicle. Secondly, they suggest that the final stages in the maturation of a retroviral core into a mature nucleoid are dependent on the detachment of the bud from its parental cell and that the driving force of budding is the association of viral transmembrane proteins with viral core proteins. An explanation is offered to account for the formation of these structures despite the phenomenon of viral interference.

Animals↗
PubMed1955

Resistance to fibroma virus infection; the role of immune leukocytes and immune macrophages.

Leukocytes and macrophages, obtained from fibroma-immune rabbits and added to immune serum-fibroma virus mixtures, significantly increased the neutralization of fibroma virus as compared with immune serum alone. Immune cell suspensions from peritoneal exudates, regional lymph nodes, buffy coats, spleen, and liver were all effective in inhibiting fibroma virus. Approximately 2000 to 4000 immune cells/mm.(3) were necessary to cause an effect but no particular cell type could be implicated as responsible for the inhibition of fibroma virus. Normal cells did not consistently and significantly inhibit fibroma virus and cells from rabbits immunized with other viruses did not inhibit fibroma virus. Studies of the mechanism of action of the immune cells revealed: (a) that living cells were essential; (b) that normal cells, sensitized with immune serum, did not simulate the effects of immune cells; (c) that immune cells contained less preformed neutralizing antibody than an equivalent volume of immune serum, and (d) that inhibition of fibroma lesions was not the result of viral interference. It is suggested that the fibroma-neutralizing effect of immune cells is related to intracellularly placed antibody or to cellular transfer of an ability to form specific antibody in recipient animals.

Animals↗
PubMed1955

Reactivation of non-infective virus in a cortisone-injected host.

The administration of cortisone to chick embryos inoculated with large quantities of inactive influenza B virus results in a rate of viral increase greater than is concommittantly observed with inocula of comparable infectivity which are devoid of inactive particles. Thus, more than a mere negation of autointerference is effected. It is concluded that in the presence of cortisone reactivation has occurred of non-infective virus to a state in which it can participate in viral synthesis. Cortisone-induced viral reactivation is dependent upon a high partide/cell ratio and is thus analogous to the previously described phenomenon of "multiplicity reactivation." Cortisone does not influence either homologous or heterologous viral interference unless reactivation of the inactive interfering virus occurs. Virus reactivable with cortisone possesses both interfering and enzymatic properties. Reactivation of virus with cortisone cannot be effected in vitro but is mediated by the host cell. Two hypotheses concerning the action of cortisone are presented.

Animals↗
PubMed1966

The influence of cortisone on experimental viral infection. VI. Inhibition by hydrocortisone of interferon synthesis in the chick embryo.

The initial observations that cortisone may act as an inhibitor of viral interference (11, 4) are now explicable as an inhibitory effect on interferon synthesis. The suggestion that the action of interferon is also inhibited by cortisone or its analogues (6) has not been confirmed in a plaque reduction type of interferon assay system in which autointerference by the challenge inoculum is a lesser problem. In this respect, the present results are in accord with those obtained by DeMaeyer and DeMaeyer (8) with hydrocortisone in a system in which a low multiplicity (0.1) Sindbis virus infection in monolayer culture was employed with cytopathic effect (CPE) as an end-point. It has been shown that hydrocortisone is restrictive to the synthesis of interferon induced by inoculation of either infective or inactivated virus into the chick embryo, and that this inhibitory effect is temporary. However, in another study in the chick embryo, three spaced injections of hydrocortisone (0.25 mg/dose) prevented the appearance of detectable interferon during the entire 64 hr observation period following inoculation of 10(3.3) EID(50) of Lee virus (12). The importance of explicit definition of experimental conditions in assessing hormonal effects on infection is illustrated by the capacity of hydrocortisone either to inhibit or increase interferon synthesis in vitro, depending on the proportion of inactivated and infective virus in the inoculum employed, and the time at which interferon is measured. As suggested previously, it is not unlikely that similar shifts in hormone-virus-interferon balance may operate in vivo to influence the outcome of infection.

Animals↗
PubMed2004

Natural HLA class I polymorphism controls the pathway of antigen presentation and susceptibility to viral evasion.

HLA class I polymorphism creates diversity in epitope specificity and T cell repertoire. We show that HLA polymorphism also controls the choice of Ag presentation pathway. A single amino acid polymorphism that distinguishes HLA-B*4402 (Asp116) from B*4405 (Tyr116) permits B*4405 to constitutively acquire peptides without any detectable incorporation into the transporter associated with Ag presentation (TAP)-associated peptide loading complex even under conditions of extreme peptide starvation. This mode of peptide capture is less susceptible to viral interference than the conventional loading pathway used by HLA-B*4402 that involves assembly of class I molecules within the peptide loading complex. Thus, B*4402 and B*4405 are at opposite extremes of a natural spectrum in HLA class I dependence on the PLC for Ag presentation. These findings unveil a new layer of MHC polymorphism that affects the generic pathway of Ag loading, revealing an unsuspected evolutionary trade-off in selection for optimal HLA class I loading versus effective pathogen evasion.

Animals↗
PubMed1981

Effect of interferon on multiplication of avian sarcoma virus B77 in duck embryo fibroblasts.

The effect of interferon on the multiplication of the avian sarcoma virus B77 in duck embryo fibroblasts was studied. The interferon used for this purpose as induced in duck embryo fibroblasts by high multiplicities of reovirus serotype 3 (strain Dearing) and purified to a specific activity of at least 2 x 10(7) units/ml (estimated to be at least 10% pure). Treatment of duck embryo fibroblasts transformed with B77 virus with as little as 50 units/ml of this interferon caused a rapid inhibition of the release of virus particles, and a decrease in the specific infectivity of the virus particles that were released of about six-fold. The protein composition of virus particles released from normal and interferon-treated duck embryo fibroblasts was not detectably different. Examination of the nature of the virus-specified proteins, as determined by precipitation with specific antisera, synthesized at various times after treatment of transformed duck embryo fibroblasts with 300 units/ml of interferon revealed the following major changes: i. a more than 5-fold increase in the amount of a protein with a molecular weight of about 100,000 (P100) precipitated by antiserum to reverse transcriptase. This increase was paralleled by a decrease in the amount of the gag-pol precursors Pr190 and Pr180, but the amount of the alpha and beta subunits of reverse transcriptase was not altered by interferon treatment. ii. An at last 3-fold increase in the amount of cell-associated gag proteins. iii. A two- to ten-fold decrease in the amount of a protein with an apparent molecular weight of 76,000, in all likelihood Pr76, precipitated by antiserum to gp85. The primary cause of the interferon-induced inhibition of virus particle release appears to be inability of Pr76 to associate with gPr95/gp85 in plasma cell membranes.

Animals↗
PubMed1985

An inhibitor of interferon action: I. Physical association of the inhibitor with interferon-gamma.

Previously, an inhibitor of interferon action has been identified in mouse lymphokine preparations. The inhibitor was produced following IFN-gamma production and thus may be involved in regulation of IFN-gamma action. We now show that native inhibitor activity as isolated from crude and partially purified IFN-gamma preparations migrates along with interferon activity on molecular sieving gels. IFN-gamma which comigrates with inhibitor migrates at a slightly higher molecular weight than IFN-gamma free of inhibitor. This inhibitor activity correlates with the decreased antiviral activity of crude IFN-gamma produced late in the course of mitogen stimulation. This is apparent for both plaque reduction and yield reduction assays for interferon. This association of IFN-gamma with its inhibitor suggests a mechanism for the local regulation of IFN-gamma activity.

Animals↗
PubMed1994

Mixed infections of hepatitis C virus as a factor in acute exacerbations of chronic type C hepatitis.

Twenty patients with chronic hepatitis C virus (HCV) infection and acute exacerbations (group A) were studied by polymerase chain reaction with genotype-specific primers to explore the role of mixed infections of HCV in acute exacerbations of chronic type C hepatitis. Another 26 patients who did not have acute exacerbation were matched controls (group B). Eleven (55%) of the group A patients had heterologous HCV, and their mean age was significantly younger than that of the 9 without heterologous infection (55 vs. 67 years, P < .05). In contrast, only 2 group B patients (7.7%) had heterologous HCV infection. In 10 of 13 patients with heterologous HCV infection, type III/2a virus emerged on type II/1b HCV, and viral interference was observed in half of them. The results support that mixed infections of HCV may be important in acute exacerbations of chronic type C hepatitis.

Acute Disease↗