Arboviruses such as West Nile virus (WNV), bluetongue virus (BTV), dengue virus (DENV) and chikungunya virus (CHIKV) infect their arthropod vectors over a range of average temperatures depending on the ambient temperature. How the transmission efficiency of an arbovirus (i.e. vector competence) varies with temperature influences not only the short term risk of arbovirus outbreaks in humans and livestock but also the long term impact of climate change on the geographical range of the virus. The strength of the interaction between viral surface (glyco)protein (GP) and the host cell receptor (Cr) on binding of virus to host cell is defined by the thermodynamic dissociation constant K_{d_receptor} which is assumed to equal 10⁻³ M (at 37 °C) for binding of a sialic acid (SA) on the arthropod midgut epithelial cell surface to a SA-binding site on the surface of BTV, for example. Here virus binding affinity is modelled with increasing number of GP/Cr contacts at temperatures from 10 °C to 35 °C taking into account the change in entropy on immobilization of the whole virus on binding (ΔS_{a_immob}). Based on published data, three thermodynamic GP/Cr binding scenarios, namely enthalpy-driven, entropy-assisted and entropy-driven, are shown to affect the temperature sensitivity of virus binding in different ways. Thus for enthalpy-driven GP/Cr binding, viruses bind host cells much more strongly at 10 °C than 35 °C. A mechanistic model is developed for the number of arthropod midgut cells with bound virus and by building in a kinetic component for the rate of arbovirus replication and subsequent spread to the arthropod salivary glands, a model for the effect of temperature on vector competence is developed. The model separates the opposing effects of temperature on midgut cell binding affinity from the kinetic component of virogenesis. It successfully accommodates both increases in vector competence with temperature as for DENV and WNV in mosquitoes and decreases as for the CHIKV 2010–1909 strain in various populations of Aedes albopictus mosquitoes. Enhanced cell binding at lower temperatures through enthalpy-driven GP/Cr binding compensates for the lower replication rate to some degree such that some transmission can still occur at lower temperatures. In contrast, the strength of entropy-driven GP/Cr binding diminishes at low temperatures although there is no minimum temperature threshold for transmission efficiency. The magnitude of ΔS_{a_immob} is an important data gap. It is concluded that thermodynamic and kinetic data obtained at the molecular level will prove important in modelling vector competence with temperature.

西尼罗河病毒（WNV），蓝舌病毒（BTV），登革热病毒（DENV）和基孔肯雅病毒（CHIKV）等虫媒病毒会根据环境温度在一定的平均温度范围内感染节肢动物。虫媒病毒的传播效率（即载体能力）如何随温度变化而变化，不仅会影响人畜中虫媒病毒爆发的短期风险，而且还会影响气候变化对病毒地理范围的长期影响。病毒与宿主细胞结合后，病毒表面（糖）蛋白（GP）与宿主细胞受体（Cr）之间相互作用的强度由热力学解离常数K _{d_receptor}定义，该常数假定为10 ^-3 例如，M（在37℃下）用于将节肢动物中肠上皮细胞表面上的唾液酸（SA）结合到BTV表面上的SA结合位点。在此，考虑到将整个病毒固定在结合体上时熵的变化（_{ΔSa_immob，}在10°C至35°C的温度下，GP / Cr接触数量增加，可以模拟病毒结合亲和力））。根据已发布的数据，显示出三种热力学GP / Cr结合方案，即焓驱动，熵辅助和熵驱动，以不同的方式影响病毒结合的温度敏感性。因此，对于由焓驱动的GP / Cr结合，病毒在10°C时比35°C结合宿主细胞的能力要强得多。建立了带有结合病毒的节肢动物中肠细胞数量的机制模型，并通过建立虫媒病毒复制和随后传播到节肢动物唾液腺的速率的动力学成分，建立了温度对载体能力影响的模型。该模型将温度对中肠细胞结合亲和力的相反影响与病毒发生的动力学成分分开。白纹伊蚊蚊。通过焓驱动的GP / Cr结合在较低温度下增强的细胞结合可以在一定程度上补偿较低的复制速率，从而在较低温度下仍可发生某些传递。相反，尽管没有最低的传输效率温度阈值，但在低温下熵驱动的GP / Cr结合强度会降低。_{ΔSa_immob}的大小是重要的数据缺口。结论是，在分子水平上获得的热力学和动力学数据将被证明对于模拟矢量随温度变化的能力很重要。