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lymphokine useful for maintaining the growth and antigenspecific cytotoxic activity of CD4+CTL clones in vitro, especially when used with T-cell growth factor.

Beyrouth, H. G. (1903). "The dengue: a study of its pathology and mode of propagation." J.Trop.Med.

Bhakdi, S. and M. D. Kazatchkine (1990). "Pathogenesis of dengue: an alternative hypothesis." Southeast Asian J.Trop.Med.public Health 21: 652-657.
This paper presents a novel but entirely hypothetical concept on the pathogenesis of the shock syndrome (DSS) associated with dengue hemorrhagic fever (DHF). Antibody-dependent enhancement (ADE) is widely thought to be central to the development of these clinical entities. Current views on the mechanisms underlying ADE centre on two major lines of thought: 1) Non-neutralizing antibodies to dengue virus (DV) can enhance viral uptake and replication in target cells (monocytes). 2) DHF/DSS are the consequences of enhanced viral replication, paired with immunopathological processes that are evoked by monocyte dysfunction and detrimental reactions caused by activated T- lymphocytes. The present hypothesis proposes, by contrast, a central role for the following processes: 1) Secondary infection of an individual who has sub or non-neutralizing antibody titers against DV leads to a booster antibody response and a steep rise in antibody levels. 2) Antibodies against DV bind to and direct a selective attack of the complement system onto cells expressing viral antigens on their surface. DHF/DSS are the direct and indirect consequences of complement activation on these cells. The advanced hypothesis, which departs from the mainstream of "immune enhancement" concepts, can easily be tested by experimentation.

Bhamarapravati, N. and V. Boonyapaknavik "Pathogenetic studies on Thai haemorrhagic fever: Immunofluorescent localization of dengue virus in human tissue." Unknown: 50-51.

Bhamarapravati, N., S. B. Halstead, et al. (1964). "Studies on dengue virus infection: I. immunofluorescent localization of virus in mouse tissue." Arch.Pathol. 77: 538-543.
SUMMARY: The application of fluorescent antibody to tissue sections was used in the study of dengue infection in newborn mice. Specific fluorescence appears about 72-96 hours after inoculation. The antigen was localized mainly in the cytoplasm of neurons and glial cells in the brain. The first appearance of antigen precedes evidence of neuronal damage and clinical disease. Cross-staining of antibody to d 1 antigen with all types of dengue antigen as well as with Japanese encephalitis virus antigen was observed. The indirect method of staining can be used for the study of antibody conversion in patients who have Thai hemorrhagic fever. Dengue antigen can be demonstrated in acetone- or formalin-fixed, paraffin-embedded sections.

Bhamarapravati, N., P. Tuchinda, et al. (1967). "Pathology of Thailand haemorrhagic fever: a study of 100 autopsy cases." Ann.Trop.Med.Parasitol. 61: 500-510.

Bhamarapravati, N., S. Yoksan, et al. (1986). Dengue virus vaccine development 2. Clinical, immunological and biological response in flavivirus immune and non-immune