Modification of the poliovirus capsid by ultraviolet light

Sena, John De; Jarvis, Donald L.

doi:10.1139/m81-183

Cited by 11 publications

(11 citation statements)

References 12 publications

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“…For UV inactivation, loss of infectivity is associated with formation of photoproducts (photodimer or photohydrate) or loss of function of the viral genomes with doses between 0.8 and 140 mW ⅐ s/cm 2 (8 and 1,400 J/m 2 ) (5,12,24,27), whereas doses of Ͼ1,000 mW ⅐ s/cm 2 (Ͼ10,000 J/m 2 ) affect the capsid protein and also generate RNA-protein linkages (3,23,28). The targets of UV on the virion are apparently dose dependent.…”

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confidence: 99%

Infectivity of RNA from Inactivated Poliovirus

Nuanualsuwan

Cliver

2003

Appl Environ Microbiol

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During inactivation of poliovirus type 1 (PV-1) by exposure to UV, hypochlorite, and heat (72°C), the infectivity of the virus was compared with that of its RNA. DEAE-dextran (1-mg/ml concentration in Dulbecco's modified Eagle medium buffered with 0.05 M Tris, pH 7.4) was used to facilitate transfecting PV-1 RNA into FRhK-4 host cells. After interaction of PV-1 RNA with cell monolayer at room temperature (21 to 22°C) for 20 min, the monolayers were washed with 5 ml of Hanks balanced salt solution. The remainder of the procedure was the same as that for the conventional plaque technique, which was also used for quantifying the PV-1 whole-particle infectivity. Plaque formation by extracted RNA was approximately 100,000-fold less efficient than that by whole virions. The slopes of best-fit regression lines of inactivation curves for virion infectivity and RNA infectivity were compared to determine the target of inactivation. For UV and hypochlorite inactivation the slopes of inactivation curves of virion infectivity and RNA infectivity were not statistically different. However, the difference of slopes of inactivation curves of virion infectivity and RNA infectivity was statistically significant for thermal inactivation. The results of these experiments indicate that viral RNA is a primary target of UV and hypochlorite inactivations but that the sole target of thermal inactivation is the viral capsid.Leading causes of food-borne, and probably water-borne, disease in the United States are the Norwalk-like viruses (NLVs) of the family Caliciviridae and the hepatitis A virus (HAV) of the family Picornaviridae (11). Poliovirus (PV) is the type species of the genus Enterovirus in the Picornaviridae family (19). PV has the same genomic structure and gene organization as that of HAV and has a close phylogenetic relationship with the NLVs (26). We have studied the inactivation of PV, HAV, and feline calicivirus (FCV, which is often used as a surrogate for NLVs because NLVs have no laboratory host cell line). Inactivating agents used in these studies were UV, hypochlorite, and heat (72°C), all of which are commonly used in food processing or preparation and in water disinfection.These simple viruses comprise only a single strand of RNA coated with protein. The RNA contains the genetic information by which intracellular infection results in production of progeny virus, so infectivity ultimately resides in the RNA. The coat protein (capsid) performs three functions: (i) protection of the RNA against environmental degradation and in transit down the digestive tract until susceptible cells are reached; (ii) attachment to the receptor of a susceptible cell, whereby the viral particle is engulfed and the capsid removed, to initiate the infection; and (iii) antigenic activity that evokes an immune response by the host and reacts with the antibody that has been produced. We have shown that capsids of HAV, vaccine PV type 1 (PV-1), and FCV inactivated (from an initial titer of ϳ1,000 PFU/ml) by UV, hypochlorite, or high temperature ...

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Infectivity of RNA from Inactivated Poliovirus

Nuanualsuwan

Cliver

2003

Appl Environ Microbiol

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“…UVinduced damage has been observed in the delta protein, an attachment protein which is analogous to VP4 of coxsackievirus and is responsible for viral adsorption (Miller & Plagemann 1974). Viral capsid structural damage and attachment ability loss caused by UVR has also been reported for several RNA viruses, such as human picornaviruses, feline calicivirus (FCV) and poliovirus (De Sena & Jarvis 1981, Nuanualsuwan & Cliver 2003. UV-damaged PV-1 (type I poliovirus) and FCV entirely lost attachment ability, indicating that inactivation required a conformational change of only a few receptor attachment sites to prevent attachment of the whole inactivated virus particle (Nuanualsuwan & Cliver 2003).…”

Section: Discussionmentioning

confidence: 82%

“…These differences in loss of attachment ability are assumed to be due to differences in the capsid (especially the receptor attachment site) (Nuanualsuwan & Cliver 2003). Besides, results obtained by De Sena & Jarvis (1981) indicate that pH and ionic compounds could affect the extent of UV damage to the attachment ability of PV-1. Taken together, these results suggest that more work needs to be performed to study UV damage to viral capsids.…”

Section: Discussionmentioning

confidence: 99%

“…UV-B may also result in the formation of reactive oxygen species (ROS) including singlet oxygen ( 1 O 2 ) or free radicals, which can destroy the structure of biological molecules such as membrane proteins and lipids (Alscher et al 1997, McKenzie et al 2003. UVR-induced capsid damage has been reported for several pathogenic RNA viruses that are released into aquatic systems through drainage systems (De Sena & Jarvis 1981, Wetz et al 1983, Nuanualsuwan & Cliver 2003. UV irradiation of type I poliovirus resulted in modification of the poliovirus capsid and loss of infectivity (De Sena & Jarvis 1981, Wetz et al 1983).…”

Section: Introductionmentioning

confidence: 99%

“…UVR-induced capsid damage has been reported for several pathogenic RNA viruses that are released into aquatic systems through drainage systems (De Sena & Jarvis 1981, Wetz et al 1983, Nuanualsuwan & Cliver 2003. UV irradiation of type I poliovirus resulted in modification of the poliovirus capsid and loss of infectivity (De Sena & Jarvis 1981, Wetz et al 1983). The primary target of UVR and other virus inactivation factors is the capsid (Nuanualsuwan & Cliver 2003).…”

Section: Introductionmentioning

confidence: 99%

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Assessment of UV-B damage in cyanophage PP

Liao¹,

Chen²,

Yang³

et al. 2010

Aquat. Microb. Ecol.

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Cyanophage PP is a short-tailed, icosahedral-shaped, double-stranded DNA virus and can be frequently detected with high abundance and activity in many eutrophic lakes in China. Solar radiation is one of the main factors affecting cyanophage infectivity. In this study, cyanophage PP was treated with different intensities of UV-B radiation, and the accumulation of cyclobutane pyrimidine dimers (CPDs), viral particle destruction and viral attachment ability were analyzed. The viral infectivity decay rate under white and red light was also studied using plaque-forming assays. The results indicate that (1) the level of CPDs induced by UV-B was significantly correlated with radiation intensity, while exposure dose had little effect on the DNA damage level, (2) the level of CPDs was significantly correlated with both the decay rate and the repair rate in cyanophage PP, and (3) UV-B could result in the destruction of viral particles and the decrease in viral attachment. This work suggests that the secondary and tertiary structure of the DNA may influence the formation of CPDs, and that capsid damage caused by UV-B radiation may play an important role in viral decay and survival.

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