Encephalomyocarditis (EMC) virus-induced diabetes mellitus prevented byCorynebacterium parvum in mice

Summary Corynebacterium parvum prevented the development of encephalomyocarditis virus-induced diabetes in mice, when it was given 3–14 days before the virus infection. This treatment inhibited virus replication in the pancreas of the infected mice at an early stage of the infection.     

Protective and immunostimulating activity of a low dose of cyclophosphamide in the experimental infection of mice with foot-and-mouth disease virus

Administration to mice of a low, non-immunosuppressive dose of cyclophosphamide 4 days before infection with foot-and-mouth disease virus decreases viral replication, enhances the immune response against the virus and prevents pancreatic damage.     

Protective and immunostimulating activity of a low dose of cyclophosphamide in the experimental infection of mice with foot-and-mouth disease virus

Summary Administration to mice of a low, non-immunosuppressive dose of cyclophosphamide 4 days before infection with foot-and-mouth disease virus decreases viral replication, enhances the immune response against the virus and prevents panceatic damage.     

Does the diabetes caused by viral infection in mice depend on immune reactions?]

Normal DBA2 mice become highly diabetic after infection with the EMC virus. But 500 R X-irradiation before infection inhibits the increase of mean blood glucose levels thus indicating the participation of immune reactions in the appearance of diabetes.     

Effectiveness of intranasal immunization with Myxovirus influenzae neuraminidase in mice]

An intranasal immunization with a A/PR8/34-isolated NA, protected mice as well as the whole virus and A/Hong Kong/1/68 virus against a subsequent infection with mice-adaptated A/PR8/34 strain.     

The influence of cold or isolation stress on resistance of mice to West Nile virus encephalitis

The effect of cold or isolation stress on mortality rate and brain virus level were investigated in mice infected with West Nile virus (WNV). Exposure of mice for 5 min/day to cold water (1 +/- 0.5 degrees C) for 8-10 days resulted in 92% mortality as compared to 47% in control mice (p less than 0.001). Mice housed in individual cages (isolation stress) were also more susceptible to WN viral infection, as shown by increased mortality rate reaching 85% as compared to 50% in mice housed 6 per cage (p less than 0.01). Cold or isolation stress increased blood brain and spleen virus levels as early as 2 days after inoculation. After 8 days of isolation or cold stress, mice inoculated with WNV had 8.9 and 9.0 log10 plaque forming units in the brain, respectively, as compared to 6.9 in the control (p less than 0.01-0.001). Furthermore, lymphoid organs such as spleen and thymus showed severe mass loss. These data suggest that physical or non-physical stress situations enhance WNV encephalitis by accelerating virus proliferation and increase mortality in mice.     

The influence of cold or isolation stress on resistance of mice to West Nile virus encephalitis

Summary The effect of cold or isolation stress on mortality rate and brain virus level were investigated in mice infected with West Nile virus (WNV). Exposure of mice for 5 min/day to cold water (1±0.5°C) for 8–10 days resulted in 92% mortality as compared to 47% in control mice (p<0.001). Mice housed in individual cages (isolation stress) were also more susceptible to WN viral infection, as shown by increased mortality rate reaching 85% as compared to 50% in mice housed 6 per cage (p<0.01). Cold or isolation stress increased blood brain and spleen virus levels as early as 2 days after inoculation. After 8 days of isolation or cold stress, mice inoculated with WNV had 8.9 and 9.0 log₁₀ plaque forming units in the brain, respectively, as compared to 6.9 in the control (p<0.01–0.001). Furthermore, lymphoid organs such as spleen and thymus showed severe mass loss. These data suggest that physical or non-physical stress situations enhance WNV encephalitis by accelerating virus proliferation and increase mortality in mice.     

The antiviral effect of Keishi-ni-eppi-ichi-to,a tranditional Chinese herbal medicine,on influenza A2(H2N2) virus infection in mice

The antiviral effect of Keishi-ni-eppi-ichi-to (TJS-064), a traditional Chinese herbal medicine, was investigation in mice infected with influenza A₂(H₂N₂) virus. When mice exposed to 5 LD₅₀ dose of the virus were treated orally with a 70 mg/kg dose of TJS-064 1 day before and 1 day and 4 days after the infection, 100% survived over a 25-day experimental period. At the end of this period all the control mice, treated with saline alone, had died; their mean survival time in days (MSD) was 11.2 days. When mice infected with a 10 LD₅₀ dose of the virus were treated with TJS-064, the MSD was >17.4 days and there was a 50% survival rate, while the control group had a MSD of 8.7 days and 0% survival rate. No significant antiviral effect TJS-064 was observed when the agent was administered orally to mice infected with a 100 LD₅₀ or large dose of influenza virus. Pulmonary consolidation, virus titers in lung tissues and HAI titers in sera of infected mice treated with TJS-064 were all significantly lower than those of infected mice treated with saline. Interferon activities were detected in sera of mice treated with the agent at a dose of 100 mg/kg orally. Since viricidal and viristatic activities of the agent against influenza virus were not demonstrated, the antiviral effects of TJS-064 may be expressed through the host's antiviral functions including interferon production.     

Protective effect of lidocaine in the experimental foot-and-mouth disease pancreatitis

Experimental infection of mice with foot-and-mouth disease virus (FMDV) induces a necrotizing pancreatitis of the exocrinar portion of the organ. The lesions are characterized by vascular congestion, edema and interstitial polymorphonuclear leukocyte (PMN) infiltrates. When infected mice were treated with different amounts of lidocaine (a local anesthetic, chemically defined as a tertiary amide compound), reduction in intensity of the pancreatic necrosis and in the number of PMN were observed. Even though lidocaine could interfere with FMDV post-replicative cytolytic mechanisms, it appears that protection against pancreatic necrosis is by attenuation of PMN presentation in the infected tissue.     

Protective effect of Shigyaku-to,a traditional Chinese herbal medicine,on the infection of herpes simplex virus type 1 (HSV-1) in mice

The antiviral activity of Shigyaku-to (TJS-109), a traditional Chinese herbal medicine, was investigated in mice infected with herpes simplex virus type 1 (HSV-1). TJS-109 is a combination of the medicinal plant extracts fromZingiberis siccatum rhizoma,Aconiti tuber andGlycyrrhizae radix in a specific proportion. Mice infected with a 10 LD₅₀ dose of HSV-1 were treated with TJS-109 orally at doses of 1.25 to 20 mg/kg 2 days before, and 1 and 4 days after the infection. The treated groups had 80% (1.25 mg/kg), 40% (5 mg/kg) and 23% (20 mg/kg) mortality rates 25 days after the infection as compared with a 100% mortality rate in control mice treated with saline. When HSV-1 infected mice (recipients) received CD8⁺T cell fractions derived from spleens of mice treated with TJS-109 (donors), 70% of recipients survived, as compared with 0% survivors in the groups of mice treated with saline, B cell fractions, CD4⁺ T cell fractions or macrophage-enriched fractions prepared from the same donors. TJS-109 did not show any virucidal activities against HSV-1 or any virostatic activities on the growth of HSV-1 in Vero cells. These results suggest that TJS-109 protected mice exposed to lethal amounts of HSV-1 through the activation of CD8⁺ T cells.     

RNA干扰CD133基因对结肠癌干细胞生物学行为的影响

目的探讨CD133基因表达、活化被阻断后对结肠癌干细胞生物学行为的影响。方法从EpcAMhighCD44＋结肠癌干细胞中流式分选获得CD133＋细胞,感染LV-CD133shRNA载体慢病毒后观察CD133＋结肠癌干细胞在生长方式、成球能力、克隆形成率、成瘤能力以及ABCC2mRNA的变化;Westernblot分析CD133-细胞中CD133蛋白表达情况。结果EpcAMhighCD44＋结肠癌干细胞中CD133＋细胞比例为89．2％。实验组经过LV-CD133shRNA载体病毒感染后,在干细胞养液中细胞改悬浮生长的方式为贴壁生长,不能形成细胞球。MTT法测定发现细胞增殖减慢,克隆形成率明显下降。将感染细胞移植在Balb／C裸鼠体内,在观察期间,感染LV—CD133shRNA载体病毒的CD133＋细胞无肿瘤形成。ABCG2mRNA表达水平明显降低（P〈0．01）。从EpcAMhighCD44＋结肠癌干细胞中流式分选获得CD133-细胞,其中也有CD133蛋白的表达。结论CD133维持结肠癌干细胞生物学特性。     

«Colony-stimulating activity» im Serum und der Milz nach Rauscher Virusinfektion

Summary Colony-stimulating activity (CSA) of serum and spleen was studied in CBA/J mice 1–5 days after Rauscher virus infection, using the agar culture system with normal mouse bone marrow cells as target cells. A sharp increase of CSA was observed with a peak after 2 days in both sites; after 5 days control levels are reached.

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Mit Unterstützung der Deutschen Forschungsgemeinschaft (SFB 112, Zellsystemphysiologie).     

In vitro proliferation of human large granular lymphocytes with v-raf/v-myc recombinant retrovirus

The effect of infection with a retrovirus carrying v-raf/v-myc oncogenes (J2 virus) on the in vitro proliferation of human large granular lymphocytes (LGL) was investigated. LGL infected with J2 virus (J2LGL), unlike uninfected cells, grew with a proliferation peak eight days after infection. Such cells retained the morphology and functional properties typical of LGL. Furthermore, 5% of J2LGL produced virus the day after infection, whereas non-virus production was detectable five days later. These data indicate that J2 virus provides a transient mitogenic signal for LGL.     

Comparison of the biological effects of anemia inducing and polycythemia inducing Friend virus complex.

The comparison of the biological effects of FVP and FVA showed that leukemogenesis appears to be delayed in FVA infected mice as compared to FVP infected animals after injection of comparable quantities of virus as measured in spleen focus forming units. In addition, no CFU-EI, characteristic for FVP induced leukemia, were found in leukemic spleen or bone marrow of FVA infected mice. Since it was possible to distinguish both viruses by their different host ranges, which are helper virus determined, it is suggested that the observed differences, especially the lack of CFU-EI in FVA infected mice, might be due to differences in the helper virus component of the FV complex.     

The implications of viral reservoirs on the elite control of HIV-1 infection

The mechanisms by which a small percentage of HIV-1 infected individuals known as elite suppressors or controllers are able to control viral replication are not fully understood. Early cases of viremic control were attributed to infection with defective virus, but subsequent work has demonstrated that infection with a defective virus is not the exclusive cause of control. Replication-competent virus has been isolated from patients who control viral replication, and studies have demonstrated that evolution occurs in plasma virus but not in virus isolates from the latent reservoir. Additionally, transmission pair studies have demonstrated that patients infected with similar viruses can have dramatically different outcomes of infection. An increased understanding of the viral factors associated with control is important to understand the interplay between viral replication and host control, and has implications for the design of an effective therapeutic vaccine that can lead to a functional cure of HIV-1 infection.     

Comparison of the biological effects of anemia inducing and polycythemia inducing Friend virus complex

Summary The comparison of the biological effects of FV^P and FV^A showed that leukemogenesis appears to be delayed in FV^A infected mice as compared to FV^P infected animals after injection of comparable quantities of virus as measured in spleen focus forming units. In addition, no CFU-EI, characteristic for FV^P induced leukemia, were found in leukemic spleen or bone marrow of FV^A infected mice. Since it was possible to distinguish both viruses by their different host ranges, which are helper virus determined, it is suggested that the observed differences, especially the lack of CFU-EI in FV^A infected mice, might be due to differences in the helper virus component of the FV complex.Supported by the Deutsche Forschungsgemeinschaft (SFB 112 Zellsystemphysiologie).     

The course ofPlasmodium berghei infection in mice latently infected withToxoplasma gondii

Summary The course of infection with 2 different virulent strains ofPlasmodium berghei was investigated in mice latently infected withToxoplasma gondii. When given the highly virulent ANKA strain ofP. berghei all Toxoplasma-infected mice died but the survival time was prolonged. After infection with the less virulent strain K 173 mice could survive the subsequent infection. In these cases levels of parasitemia depended upon the duration of theT. gondii infection. Mice infected for about 6 weeks withT. gondii showed maximum protection. These studies were conducted in the Institut für Medizinische Parasitologie der Universit?t Bonn (D-5300 Bonn, Federal Republic of Germany).     

In vitro transmission of mouse leukemia virus to restrictive mouse cells: necessity for mixed infection by two different leukemia viruses]

The plaque formation of murine leukemia virus (MuLV) in non permissive mouse cells (N-tropic MuLV in B-type cells, or B-tropic MuLV in N-type cells) was increased by murine sarcoma virus whose plaque-forming activity was extremely low (MuSV XC-). The infection of N-tropic MuLV in B-type cells was increased by MuSV XC- propagated only in N-type cells but not in B-type cells, and the infection of B-tropic MuLV in N-type cells by MuSV XC- propagated only in B-type cells but not in N-type cells.     

An antiviral factor from Melia azedarach L. prevents Tacaribe virus encephalitis in mice

Treatment of neonatal mice with an antiviral factor, (AVF), obtained from the leaves of Melia azedarach L. protected them against lethal encephalitis caused by Tacaribe virus inoculation. The degree of protection obtained varied from 66% to 100% depending on the virus dose. Similarly, administration of AVF to nursing mothers protected their offspring from developing virus encephalitis. AVF does not directly inactivate Tacaribe virus; it inhibits an early step (s) in the replication process in cell cultures.     

Systemic candidiasis from Candida albicans colonizing the gastrointestinal tract of mice.

Reproducible induction of systemic Candida infection was achieved by treating mice in which Candida colonization had been established in the gastrointestional tract by aminobenzylpenicillin treatment. Systemic candidiasis was induced in these mice by X-ray irradiation followed by immunosuppressive doses of dexamethasone or X-ray irradiation followed by immunosuppressive doses of trypan blue. Macrophages seem to play an important role in thie systemic infection.