It is quite possible that the silk proteins synthesized by their common ancestor were already composed of highly homogenized tandem repeats, suggesting that this type of molecular organization is a fundamental prerequisite for silk fiber production. Lastly it would be interesting to evaluate the relationship between the evolution of molecular complexity and its association with the evolution of anatomical and behavioral complexity in spiders. While Actinopodidae spiders use their webs only to coat their burrows and surroundings, G. cancriformis and orb-weaver spiders in general use webs made from different spidroin molecules in different ecological and behavioral contexts. An intriguing question is which complexity augmenting factor arose first: the anatomical; the behavioral; or the molecular? In a scenario in which behavioral modification appeared first, one can imagine that soon the spider would be under selective pressure at the molecular level to produce different types of silk with different amounts of resistance and elasticity. At that moment, the random process of gene duplication might have occurred, allowing further subfunctionalization of the spidroin genes. If this event did take place, it would probably be positively selected for. In this scenario, the last step after the increase of behavioral and molecular complexity would be the anatomical subfunctionalization, during which a new or existent part of an original spinning gland would specialize in producing a single type of silk. The finding of fibroins and MaSps in mygalomorphs is an evidence that spidroin gene duplications happened before the anatomical specialization of spinning glands. Surely these hypothesized gene duplications and subfunctionalizations would need to be accompanied by differences in regulatory sequences related to the specific transcription of silk mRNAs too. This hypothesis will be better investigated after the complete sequencing of a number of spider genomes. The virus can cause flu-like symptoms that may progress to dengue hemorrhagic fever and dengue shock syndrome. Dengue fever is characterized by a rapid onset of fever, headache, muscle and joint pain. During a primary infection, most cases are self-limiting. There exist four genetically related serotypes of dengue virus. Infection with one serotype induces lifelong immunity to the homologous serotype. However, after infection with a second different serotype, the cross-reacting non-neutralizing antibodies against the first serotype will recognize the heterologous virus and enhance DENV access to Fc-receptor bearing cells. This phenomenon is called antibodydependent enhancement and leads to a higher viremia, increased vascular permeability and a severe hemorrhagic disease. The first reported epidemic of DHF occurred in the Philippines in 1953. The past two decades, the global incidence of dengue fever has increased dramatically. Reasons for the spread of dengue virus are the expansion of global population and travelling, deforestation, solid waste systems and poor vector control. The latter one is the only weapon against dengue virus, since there is no antiviral drug or vaccine available. Clinical studies with tetravalent chimeric dengue virus vaccines are ongoing. Following the bite of an infected mosquito, Diperodon immature dendritic cells in the skin are believed to be the first target cells during DENV infection. Several cellular receptors for DENV have been Catharanthine sulfate proposed: heparan sulfate, LPS/CD14-associated binding proteins.