Viruses Virulent

The expression at early and late times post-infection of an abundantly secreted vCKBP-2 might be expected to make a significant contribution to virus virulence in vivo by inhibiting CC-chemokine-mediated host inflammatory responses. Surprisingly, the experimental evidence currently available indicates that vCKBP-2 has only marginal effects on poxvirus virulence. 

Ng A, Tscharke DC, Reading PC et al. The vaccinia virus A4lL protein is a soluble 30 kDa glycoprotein that affects virus virulence. J Gen Virol 2001 82 2095-2105. 

Reading PC, Khanna A, Smith GL. Vaccinia virus CrmE encodes a soluble and cell surfiice tumor necrosis factor receptor that contributes to virus virulence. Virology 2002 292(2) 285-298. 

Cooray S, Bahar MW, Abrescia NG et al. Functional and structural studies of the vaccinia virus virulence factor N1 reveal a Bcl-2-like anti-apoptotic protein.) Gen Virol 2007 88(Pt 6) 1656-1666. 

Upton QMaccnJL, Wishart OS ctaL Myxoma virus and malignant rabbit fibroma virus encode a serpin-like protein important for virus virulence. Virology 1990 179 618431. 

The contribution of gG to virus virulence has been addressed in several models of alphaherpesvi-rus infitetion. The infection of mice with low doses of an EHV-1 gG mutant led to an exacerbation... 

Reading PC, Symons JA, Smith GL. A soluble chemokine-binding protein from vaccinia virus reduces virus virulence and the inflammatory response to infection. J Immunol 2003 170(3) 1435-1442. 

Price N, Tscharke DC, Hollinshead M et al. Vaccinia virus gene B7R encodes an 18-kOa protein that is resident in the endoplasmic reticulum and affects virus virulence. Virology 2000 267(l) 65-79. 

Ng, A., Tscharke, D.C., Reading, P.C., and Smith, G.L. (2001) The vaccinia virus A41L protein is a soluble 30kDa glycoprotein that affects virus virulence. The Journal of General Virology, 82, 2095-2105. 

Wild-type virus. If virus virulence is less than wild-type, a lower containment level may be used. 

With attenuated viral vaccines the potential hazards are those associated with reversion of the virus during production to a degree of virulence capable of causing disease in vaccinees. To a large extent this possibility is controlled by very careful selection of a stable seed but, especially with live attenuated poliomyelitis vaccine, it is usual to compare the neurovirulence of the vaccine with that of a vaccine known to be safe in field use. The technique involves the intraspinal inoculation of monkeys with a reference vaccine and with the test vaccine and a comparison ofthe neurological lesions and symptoms, if any, that are caused. If the vaccine causes abnormalities in excess of those caused by the reference it fails the test. 

Propagated outbreaks of infection relate to the direct transmission of an infective agent from a diseased individual to a healthy, susceptible one. Mechanisms of such transmission were described in Chapter 4 and include inhalation of infective aerosols (measles, mumps, diphtheria), direct physical contact (syphilis, herpes virus) and, where sanitation standards are poor, through the introduction of infected faecal material into drinking water (cholera, typhoid). The ease oftransmission, and hence the rate of onset of an epidemic (Fig. 16.3) relates not only to the susceptibility status, and general state of health of the individuals but also to the virulence properties of the organism, the route oftransmission, the duration of the infective period associated with the disease. 

Faecal excretion of vaeeine virus will oeeur and may last for up to 6 weeks. Such released virus will spread to elose eontaets and infect/(re)immunize them. Since the introduction of OPV, notifications of paralytic poliomyelitis in the UK have dropped speetacularly. From 1985-95, 19 of the 28 notified cases of paralytic poliomyelitis were associated with vaeeine strains (14 reeipients, 5 contacts). Vaccine-associated poliomyelitis may occur through reversion of the attenuated strains to the virulent wild-... 

The temperate virus does not exist in its mature, infectious state inside the cell, but rather in a latent form, called the provirus or prophage state. In considering virulent viruses we learned that the DNA of the virulent virus contains information for the synthesis of a number of enzymes and other proteins essential to virus reproduction. The prophage of the temperate virus carries similar information, but in the lysogenic cell this information remains dormant because the expression of the virus genes is blocked through the action of a specific repressor coded for by the virus. As a result of a genetic switch, the repressor is inactivated, virus reproduction occurs, the cell lyses, and virus particles are released. 

Mink enteritis virus VP2 epitope Epitope display on cowpea mosaic virus in cowpea leaf Immunogenic in mink when delivered parenterally. Protective against challenge with virulent MEV. 82... 

Foot and mouth disease virus (FMDV) VP1 epitope Arabidopsis leaf Serum antibodies reacted strongly with intact FMDV particles. Immunogenic in mice when administered parenterally. Protective against challenge with virulent FVDM. 93... 

Infectious bronchitis virus (IBV) SI glycoprotein Potato tuber Antibodies neutralized IBV from mice and chickens. Immunogenic in chickens when administered orally, nasally, and parenterally. Protective after 3 immunizations in chickens when challenged with virulent IBV. 103... 

Rabbit hemorrhagic disease virus VP60 epitope Potato leaf VP60 specific antibodies elicited in rabbits. Immunogenic in rabbits when administered parenterally. Rabbits protected when challenged with virulent RDHV. 67... 

Mild form of smallpox caused by a less virulent form of the virus. The toxemia is less, lesions are more superficial, and healing time was more rapid. The natural reservoir is humans. This is a biosafety level 4 agent. 

A number of approaches are being assessed with regard to developing an effective AIDS vaccine. No safe attenuated form of the virus has been recognized to date, nor is one likely to be developed in the foreseeable future. The high level of mutation associated with HIV would, in any case, heighten fears that spontaneous reversion of any such product to virulence would be possible. 

The life cycle of many viruses, including retroviruses, depends on viral proteases that cleave viral glycoproteins into individual polypeptides, and these enzymes are necessary for viral replication. NO can inactivate coxsackievirus [136]. Since cysteine proteases are critical for the virulence and replication of many viruses, nitrosation of viral cysteine proteases may be a mechanism of antiviral host defense. NO mediates nitrosation of cysteine and aspartyl proteases of HIV-1, and it was suggested that this... 

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