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At least 91 records · Page 5Linked to original sources
PubMed2001

A mathematical model describing the thermal virus inactivation.

A new mathematical model is proposed to describe the inactivation of viruses at different temperatures. This model takes into account the exponential decrease of the viral titer with time, the inactivation rate being an exponential function of the temperature. A one-step non-linear regression was used to fit oral poliovirus vaccine (OPV) experimental data. In one of the applications of the model, we illustrate the use of our model to compare the accelerated degradation test of OPV new formulations to standard OPV. Such a model is both simple and convenient to use. It should be a useful tool in optimizing formulations for live viral vaccines.

Drug Stability↗
PubMed2006

Resistance of porcine circovirus and chicken anemia virus to virus inactivation procedures used for blood products.

BACKGROUND: Virus inactivation procedures are used to prevent contamination of plasma-derived blood products with viruses. Pasteurization or prolonged dry heat has proven effective against several enveloped and nonenveloped viruses and provides an additional layer of safety for plasma products. STUDY DESIGN AND METHODS: The resistance of porcine circovirus 2 (PCV2) and chicken anemia virus (CAV), two small, nonenveloped viruses, to standard (pasteurization, 10 hr at 60 degrees C; dry heating, 80 degrees C for 72 hr) and more extreme heat inactivation procedures (temperatures up to 120 degrees C) was determined. The ability of these procedures to inactivate PCV2 and CAV was measured by comparison of in vitro infectivity before and after treatment. RESULTS: Infectivity of PCV2 and CAV was reduced by approximately 1.6 and 1.4 log by pasteurization and by 0.75 and 1.25 log by dry-heat treatment, both substantially more resistant than other viruses previously investigated. PCV2 and CAV were additionally almost completely resistant to dry-heat treatment up to 120 degrees C for 30 minutes (mean log infectivity reductions, 1.25 and 0.6), although both were more effectively inactivated when the temperature of wet-heat treatment was increased to 80 degrees C (>3.2 and >3.6 log infectivity reduction). CONCLUSION: Although neither PCV2 nor CAV are known to infect humans, their inactivation properties may represent those of other small DNA viruses known to be present (e.g., TT virus, small anellovirus) or potentially present in human plasma. Findings of extreme thermal resistance demonstrate that recipients of plasma-derived therapeutics may potentially still be exposed to small DNA viruses, despite the implementation of viral inactivation steps.

Animals↗
PubMed1997

Effect of two virus inactivation methods: electron beam irradiation and binary ethylenimine treatment on determination of reproductive hormones in equine plasma.

Ionizing irradiation and binary ethylenimine treatment have previously been shown to be effective for in-vitro inactivation of virus in biological material. In the present study the 2 methods were tested for possible effects on measurable concentrations of reproductive hormones in equine plasma (luteinizing hormone (LH), folliclestimulating hormone (FSH), progesterone (P4), and oestradiol-17 beta (E2)). The inactivation methods were electron beam irradiation with a dose from 11 to 44 kGy or treatment with binary ethylenimine (BEI) in concentrations of 1 and 5 mmol/L. Generally, there was a close correlation (r > 0.8, < 0.001) between pre- and post-treatment hormone levels. Thus, the different phases of the oestrous cycle could be distinguished on the basis of measured hormone concentrations of treated samples. However, both treatments significantly changed hormone concentrations of the plasma samples. For LH, FSH, and E2 the effect of irradiation and BEI treatment was depressive and dose-dependent. For P4 the effect of irradiation was also depressive and dose-dependent. However, the highest dose of BEI resulted in an increase of measured P4 concentration, which may be attributed to changes in the plasma matrix due to the treatment. Although the treatments affected measured hormone concentrations, the close correlation between pre-treatment and post-treatment measurements means that the diagnostic value will remain unchanged.

Animals↗
PubMed1998

Patterns of hepatitis G viraemia and liver disease in haemophiliacs previously exposed to non-virus inactivated coagulation factor concentrates.

Hepatitis G virus (HGV), a novel flavivirus, has been implicated as a cause of posttransfusion hepatitis. We have performed a longitudinal study in a cohort of haemophiliacs (n = 68) who previously received non-virus inactivated coagulation factor concentrates to assess both patterns of HGV viraemia and any associated liver disease. Hepatitis C virus (HCV) RNA was present in 58/68 and co-infection with human immunodeficiency virus (HIV) was present in 15/68. HGV RNA was detected in 17/68 (25%) samples from the mid-1980s. There was no association between either HIV infection (p = 0.74) or co-infection with a particular HCV genotype (p = 0.62). However, there was a relationship between HGV viraemia and the severity of haemophilia (p = 0.0004) with HGV RNA detected in 5/19, 9/16 and 3/32 patients with mild, moderate and severe haemophilia respectively. A longitudinal study was performed in 15/17 haemophiliacs with HGV viraemia using stored serum samples from the 1980s and 1990s. HGV viraemia persisted in 8/15 and cleared in 7/15 over a variable period of time. A Weibull model was constructed to estimate the duration of HGV viraemia in the study group. The 75th and 90th percentiles for the duration of HGV were estimated to be 8.7 years (95%, confidence interval 4.8-15.7) and 23.6 years (95% confidence interval 11.8-47.1) respectively. Laparoscopic liver inspection/biopsy was performed in 25/68. There was no association between severity of liver disease and HGV viraemia (p = 0.43). This study demonstrates considerable variation in patterns of HGV viraemia in haemophiliacs. We found little evidence to implicate HGV as a major cause of chronic liver disease in haemophiliacs.

Adolescent↗
PubMed1989

Progress in purification of virus-inactivated factor VIII concentrates. Three generations of solvent/detergent treated plasma derivatives.

A production process of a newly developed highly purified and virus-inactivated Factor (F) VIII-concentrate (Octa V.I. and Octavi) is presented. Taking advantage of a selective resin matrix and the solvent/detergent procedure for virus inactivation--known not to denaturate proteins--a product of a specific activity greater than or equal to 100 IU F VIII/mg could be developed in the final container without the use of an immuno-affinity adsorption step. The main steps of the procedure are: Pooled cryoprecipitate is extracted, the extract is cleared from fibrinogen at + 10 degrees C and virus-inactivated at + 28 degrees C after addition of tributyl-phosphate (TNBP) and detergent. Thereafter the extract is brought in contact to a F VIII-selective anion exchange resin using a chromatographic column. TnBP and the detergent are removed by an extensive washing process and the F VIII-activity is concentrated in a fraction, ready for filling, by means of a cascade of wahing- and elution-buffers. The product is free from coagulable protein and gamma-globulins. The F VIIIC: Ag/F VIII:C-ratio is about unity, suggesting the F VIII-molecule remained in its native state. The development of highly purified F VIII concentrate is based on two previous products of lesser purity (spec. activity of about 1 and 10 IU/mg). The evolution is shown by a comparison of detailed analytical data.

Chromatography, Ion Exchange↗
PubMedDate not supplied

Euphorbia thymifolia suppresses herpes simplex virus-2 infection by directly inactivating virus infectivity.

1. The ethyl acetate (EtOAc) extract and 3-O-galloyl-4,6-(S)-hexahydroxydiphenoyl-d-glucose (3OG46HG) of Euphorbia thymifolia Linnea have been shown to exhibit anti-herpes simplex virus (HSV)-2 activity in vitro. In the present study, we investigated the mode of action of these two compounds in suppressing HSV-2 multiplication. 2. The results demonstrated that the EtOAc extract and 3OG46HG affected virus infectivity in a dose-dependent manner. The EtOAc extract significantly reduced virus infectivity at a concentration of 4.0 microg/mL, whereas 3OG46HG obviously diminished virus infectivity at concentration of a 0.5 microg/mL. The virucidal ability of the EtOAc extract was affected by the incubation period, but not by the incubation temperature. In the case of the action of 3OG46HG against HSV-2, the effects of incubation time and temperature were negligible. 3. In summary, the EtOAc extract and 3OG46HG of E. thymifolia are concluded to inhibit HSV-2 multiplication by reducing virus infectivity.

Animals↗
PubMed2000

Vaccination with inactivated virus but not viral DNA reduces virus load following challenge with a heterologous and virulent isolate of feline immunodeficiency virus.

It has been shown that cats can be protected against infection with the prototypic Petaluma strain of feline immunodeficiency virus (FIV(PET)) using vaccines based on either inactivated virus particles or replication-defective proviral DNA. However, the utility of such vaccines in the field is uncertain, given the absence of consistent protection against antigenically distinct strains and the concern that the Petaluma strain may be an unrepresentative, attenuated isolate. Since reduction of viral pathogenicity and dissemination may be useful outcomes of vaccination, even in the absence of complete protection, we tested whether either of these vaccine strategies ameliorates the early course of infection following challenge with heterologous and more virulent isolates. We now report that an inactivated virus vaccine, which generates high levels of virus neutralizing antibodies, confers reduced virus loads following challenge with two heterologous isolates, FIV(AM6) and FIV(GL8). This vaccine also prevented the marked early decline in CD4/CD8 ratio seen in FIV(GL8)-infected cats. In contrast, DNA vaccines based on either FIV(PET) or FIV(GL8), which induce cell-mediated responses but no detectable antiviral antibodies, protected a fraction of cats against infection with FIV(PET) but had no measurable effect on virus load when the infecting virus was FIV(GL8). These results indicate that the more virulent FIV(GL8) is intrinsically more resistant to vaccinal immunity than the FIV(PET) strain and that a broad spectrum of responses which includes virus neutralizing antibodies is a desirable goal for lentivirus vaccine development.

Animals↗
PubMed2001

In vitro human immunodeficiency virus eradication by autologous CD8(+) T cells expanded with inactivated-virus-pulsed dendritic cells.

Despite significant immune recovery with potent highly active antiretroviral therapy (HAART), eradication of human immunodeficiency virus (HIV) from the bodies of infected individuals represents a challenge. We hypothesized that an inadequate or inappropriate signal in virus-specific antigen presentation might contribute to the persistent failure to mount efficient anti-HIV immunity in most HIV-infected individuals. Here, we conducted an in vitro study with untreated (n = 10) and HAART-treated (n = 20) HIV type 1 (HIV-1) patients which showed that pulsing of monocyte-derived dendritic cells (DC) with aldrithiol-2-inactivated autologous virus resulted in the expansion of virus-specific CD8(+) T cells which were capable of killing HIV-1-infected cells and eradicating the virus from cultured patient peripheral blood mononuclear cells independently of the disease stages and HAART response statuses of the patients. This in vitro anti-HIV effect was further enhanced by the HIV protease inhibitor indinavir (at a nonantiviral concentration), which has been shown previously to be able to up-regulate directly patient T-cell proliferation following immune stimulation. However, following a 2-day treatment with culture supernatant derived from immune-activated T cells (which mimics an in vivo environment of HIV-disseminated and immune-activated lymphoid tissues), DC lost their capacity to present de novo inactivated-virus-derived antigens. These findings provide important information for understanding the establishment of chronic HIV infection and indicate a perspective for clinical use of DC-based therapeutic vaccines against HIV.

Anti-HIV Agents↗
PubMed1997

Virus inactivation and prevalence of GBV-C in haemophiliacs.

A new putative hepatitis virus has recently been discovered and termed GB virus C (GBV-C). We investigated the prevalence of this virus among 50 haemophiliacs treated with non-virus-inactivated clotting factor concentrates prior to 1985 and 21 haemophiliacs treated exclusively with virus-inactivated clotting factor concentrates. In the first group the prevalence of GBV-C based on PCR and ELISA was 46%. In the second group the prevalence of GBV-C was similar to that of healthy blood donors (5%). We therefore conclude that GBV-C is reliably inactivated by modern virucidal methods such as vapour heating, pasteurization and treatment with solvent/detergent mixtures.

Blood Coagulation Factors↗