Dense Particles and Slow Sedimenting Particles Produced by Ultraviolet Irradiation of Poliovirus

Wetz, Klaus; Zeichhardt, Heinz; Willingmann, Peter; Habermehl, K. O.

doi:10.1099/0022-1317-64-6-1263

Cited by 15 publications

(17 citation statements)

References 25 publications

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“…HAV and PV have often been transmitted via food and water (5), and FCV is the best available surrogate for the NLVs (10), which are leading causes of food-borne and waterborne disease in the United States. As was stated earlier, the choice of inactivating agents for this study was based partly on the knowledge that UV predominantly targets the viral RNA, depending on the dose (14,39), and hypochlorite is supposed to affect both the coat protein and the RNA (1,26,40). It was somewhat surprising to find that UV, hypochlorite, and 72°C inactivation significantly attack the capsid, whereby the capsid becomes susceptible to RNase in conjunction with PK (also representing the proteolytic enzymes in the intestine) and can no longer protect the viral RNA (25).…”

Section: Discussionmentioning

confidence: 99%

“…Inactivation at 37°C was intended to represent the fate of the majority of viruses that lose infectivity in the environment, without human intervention. These inactivating agents were expected to represent different modes of attack: high-temperature heat principally attacks the viral coat protein (4), UV predominantly targets the viral RNA, depending on the dose (14,39), and hypochlorite is supposed to affect both the coat protein and the RNA (1,26,40). At moderate temperatures (Յ37°C), the RNA is probably the labile moiety.…”

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confidence: 99%

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Capsid Functions of Inactivated Human Picornaviruses and Feline Calicivirus

Nuanualsuwan

Cliver

2003

Appl Environ Microbiol

160

135

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The exceptional stability of enteric viruses probably resides in their capsids. The capsid functions of inactivated human picornaviruses and feline calicivirus (FCV) were determined. Viruses were inactivated by UV, hypochlorite, high temperature (72°C), and physiological temperature (37°C), all of which are pertinent to transmission via food and water. Poliovirus (PV) and hepatitis A virus (HAV) are transmissible via water and food, and FCV is the best available surrogate for the Norwalk-like viruses, which are leading causes of food-borne and waterborne disease in the United States. The capsids of all 37°C-inactivated viruses still protected the viral RNA against RNase, even in the presence of proteinase K, which contrasted with findings with viruses inactivated at 72°C. The loss of ability of the virus to attach to homologous cell receptors was universal, regardless of virus type and inactivation method, except for UV-inactivated HAV, and so virus inactivation was almost always accompanied by the loss of virus attachment. Inactivated HAV and FCV were captured by homologous antibodies. However, inactivated PV type 1 (PV-1) was not captured by homologous antibody and 37°C-inactivated PV-1 was only partially captured. The epitopes on the capsids of HAV and FCV are evidently discrete from the receptor attachment sites, unlike those of PV-1. These findings indicate that the primary target of UV, hypochlorite, and 72°C inactivation is the capsid and that the target of thermal inactivation (37°C versus 72°C) is temperature dependent.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Capsid Functions of Inactivated Human Picornaviruses and Feline Calicivirus

Nuanualsuwan

Cliver

2003

Appl Environ Microbiol

160

135

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“…The present study was undertaken to determine whether the RNA in viruses inactivated by various means had retained its infectious potential. Only PV was used in these experiments, because we were unable to infect cells with RNA from the other two viruses under the conditions shown to work with PV.The UV dose to inactivate 90% of PFU (1 log 10 of inactivation) of PV/milliliter is about 0.96 mW ⅐ s/cm 2 (9.6 J/m 2 ) in clear suspending medium (29) and is between 0.377 and 0.745 mW ⅐ s/cm 2 (3.77 and 7.45 J/m 2 ) in estuarine water and seawater, respectively (6, 7); a decimal inactivation dose of 24.1 mW ⅐ s/cm 2 (241 J/m 2 ) for PV-1 in phosphate-buffered saline (PBS) was recently reported (16). For hypochlorite inactivation at pH ϳ7.0, the CϫT (concentration ϫ time) values (in milligrams per liter per minute) to inactivate 90% of PV-1 are ca.…”

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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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“…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%

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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Dense Particles and Slow Sedimenting Particles Produced by Ultraviolet Irradiation of Poliovirus

Cited by 15 publications

References 25 publications

Capsid Functions of Inactivated Human Picornaviruses and Feline Calicivirus

Capsid Functions of Inactivated Human Picornaviruses and Feline Calicivirus

Infectivity of RNA from Inactivated Poliovirus

Assessment of UV-B damage in cyanophage PP

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