Success of Selection in Terms of Hygienic Behavior in Struggle Against DWV and Varroa

Many studies have reported sudden and large-scale losses in honey bee colonies. There is no precise explanation for this happening, but it may be caused by the interaction of pathogenic viruses and ectoparasite Varroa destructor. Deformed-wing virus (DWV) is common in Apis mellifera L. and has been implicated in worldwide Varroa-associated colony losses. Hygienic behavior may be one of the ways that limit V. destructor infestation level and DWV load. The purpose of this research was to determine whether the selection of higher hygienic behavior is effective against V. destructor and DWV. Workers and pupae of A. m. anatoliaca were collected from colonies showing four generations of hygienic behaviodr, and non-hygienics were used as a control. Loads of DWV were investigated by one-step RT-qPCR, and the bottom-board method was used to allow mites count. The prevalence of DWV in pupae were higher in hygienic colonies (69.0%, average viral load 234.38) than control colonies (60.8% average viral load 937.70). However, the prevalence of worker bees infected with DWV was lower in hygienic colonies (41.3%, average viral load 181627.69) than in control's (66.0%, average viral load 241982.35). Although the averages of the Varroa counts were significantly different for both hygienic (28.92) and control colonies (108.90), we could not find any correlation between DWV loads of both workers and pupae in this study. When all these results are evaluated, the selection performed in terms of hygienic behavior can said to have been said successful against DWV.

Defining Kinetic Properties of HIV-Specific CD8+ T-Cell Responses in Acute Infection

Multiple lines of evidence indicate that CD8 + T cells are important in the control of HIV-1 (HIV) replication. However, CD8 + T cells induced by natural infection cannot eliminate the virus or reduce viral loads to acceptably low levels in most infected individuals. Understanding the basic quantitative features of CD8 + T-cell responses induced during HIV infection may therefore inform us about the limits that HIV vaccines, which aim to induce protective CD8 + T-cell responses, must exceed. Using previously published experimental data from a cohort of HIV-infected individuals with sampling times from acute to chronic infection we defined the quantitative properties of CD8 + T-cell responses to the whole HIV proteome. In contrast with a commonly held view, we found that the relative number of HIV-specific CD8 + T-cell responses (response breadth) changed little over the course of infection (first 400 days post-infection), with moderate but statistically significant changes occurring only during the first 35 symptomatic days. This challenges the idea that a change in the T-cell response breadth over time is responsible for the slow speed of viral escape from CD8 + T cells in the chronic infection. The breadth of HIV-specific CD8 + T-cell responses was not correlated with the average viral load for our small cohort of patients. Metrics of relative immunodominance of HIV-specific CD8 + T-cell responses such as Shannon entropy or the Evenness index were also not significantly correlated with the average viral load. Our mathematical-model-driven analysis suggested extremely slow expansion kinetics for the majority of HIV-specific CD8 + T-cell responses and the presence of intra- and interclonal competition between multiple CD8 + T-cell responses; such competition may limit the magnitude of CD8 + T-cell responses, specific to different epitopes, and the overall number of T-cell responses induced by vaccination. Further understanding of mechanisms underlying interactions between the virus and virus-specific CD8 + T-cell response will be instrumental in determining which T-cell-based vaccines will induce T-cell responses providing durable protection against HIV infection.

Defining Kinetic Properties of HIV-Specific CD8+ T-cell Responses in Acute Infection

Multiple lines of evidence indicate that CD8$^+$ T cells are important in the control of HIV-1 (HIV) replication. However, CD8$^+$ T cells induced by natural infection cannot eliminate the virus or reduce viral loads to acceptably low levels in most infected individuals. Understanding the basic quantitative features of CD8$^+$ T-cell responses induced during the course of HIV infection may therefore inform us about the limits that HIV vaccines, which aim to induce protective CD8$^+$ T-cell responses, must exceed. Using previously published experimental data from a cohort of HIV-infected individuals with sampling times from acute to chronic infection we defined the quantitative properties of CD8$^+$ T-cell responses to the whole HIV proteome. In contrast with a commonly held view, we found that the relative number of HIV-specific CD8$^+$ T-cell responses (response breadth) changed little over the course of infection (first 400 days post-infection), with moderate but statistically significant changes occurring only during the first 35 symptomatic days. This challenges the idea that a change in the T-cell response breadth over time is responsible for the slow speed of viral escape from CD8$^+$ T cells in the chronic infection. The breadth of HIV-specific CD8$^+$ T-cell responses was not correlated with the average viral load for our small cohort of patients. Metrics of relative immunodominance of HIV-specific CD8$^+$ T-cell responses such as Shannon entropy or the Evenness index were also not significantly correlated with the average viral load. Our mathematical-model-driven analysis suggested extremely slow expansion kinetics for the majority of HIV-specific CD8$^+$ T-cell responses and the presence of intra- and interclonal competition between multiple CD8$^+$ T-cell responses; such competition may limit the magnitude of CD8$^+$ T-cell responses, specific to different epitopes, and the overall number of T-cell responses induced by vaccination. Further understanding of mechanisms underlying interactions between the virus and virus-specific CD8$^+$ T-cell response will be instrumental in determining which T-cell-based vaccines will induce T-cell responses providing durable protection against HIV infection.

Defining kinetic properties of HIV-specific CD8+T-cell responses in acute infection

Multiple lines of evidence indicate that CD8+T cells are important in the control of HIV-1 (HIV) replication. However, CD8+T cells induced by natural infection cannot eliminate the virus or reduce viral loads to acceptably low levels in most infected individuals. Understanding the basic quantitative features of CD8+T-cell responses induced during the course of HIV infection may therefore inform us about the limits that HIV vaccines, which aim to induce protective CD8+T-cell responses, must exceed. Using previously published experimental data from a cohort of HIV-infected individuals with sampling times from acute to chronic infection we defined the quantitative properties of CD8+T-cell responses to the whole HIV proteome. In contrast with a commonly held view, we found that the relative number of HIV-specific CD8+T-cell responses (response breadth) changed little over the course of infection (first 400 days post-infection), with moderate but statistically significant changes occurring only during the first 35 symptomatic days. This challenges the idea that a change in the T-cell response breadth over time is responsible for the slow speed of viral escape from CD8+T cells in the chronic infection. The breadth of HIV-specific CD8+T-cell responses was not correlated with the average viral load for our small cohort of patients. Metrics of relative immunodominance of HIV-specific CD8+T-cell responses such as Shannon entropy or the Evenness index were also not significantly correlated with the average viral load. Our mathematical-model-driven analysis suggested extremely slow expansion kinetics for the majority of HIV-specific CD8+T-cell responses and the presence of intra- and interclonal competition between multiple CD8+T-cell responses; such competition may limit the magnitude of CD8+T-cell responses, specific to different epitopes, and the overall number of T-cell responses induced by vaccination. Further understanding of mechanisms underlying interactions between the virus and virus-specific CD8+T-cell response will be instrumental in determining which T-cell-based vaccines will induce T-cell responses providing durable protection against HIV infection.AbbreviationsCTLcytotoxic T lymphocyteHIVhuman immunodeficiency virusSEShannon entropyEIEvenness indexPBMCperipheral blood mononuclear cellsSFCspot-forming cellsIFNinterferon