Effect of human immunodeficiency virus type-1 envelope glycoprotein gp160 on cytokine production from cord-blood T cells

We have recently demonstrated that the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein gp160 enhances the in vitro differentiation of hematopoietic myeloid progenitor cells derived from cord blood by inducing secretion of colony-stimulating factor(s) (CSF) in T cells, presumably through the interaction of gp160 with CD4 molecules. In this study, we investigated the gp 160-induced humoral CSFs in cord blood by enzyme-linked immunosorbent assay (ELISA) and by polymerase chain reaction on reverse-transcribed mRNA (RT-PCR). We demonstrate that gp160 can induce interleukin (IL)-3, IL-6, and granulocyte-macrophage CSF (GM-CSF) protein secretion only in purified cord-blood T cells (CB-T) and not in detectable amounts in whole cord blood cells (WCB); cytokine mRNA induction occurred in purified CB-T and WCB, but was significantly greater in the former. Treatment of gp160 with soluble CD4 (sCD4) abolished the secretion of all three cytokines in CB-T cells, which suggests that interaction of gp160 with CD4 molecules is required for the secretion of these cytokines from CB- T cells. However, in WCB cells, sCD4 treatment of gp160 resulted in inhibition of only IL-3 and GM-CSF mRNA, whereas IL-6 secretion was enhanced. Purified cord-blood monocytes secreted only IL-6 in response to gp160, and the gp160-induced IL-6 secretion by monocytes was also further increased by gp160 + sCD4 complex. Furthermore, monocyte culture supernatants suppressed gp160-induced IL-3 secretion from CB-T cells. These findings indicate that (1) CB-T cells are a potent source of gp160-induced hematopoietic cytokines, and (2) that different mechanisms are involved in the induction of IL-6 by gp160 in the T- and non-T-cell fractions of cord blood. The ability of HIV gp160 to induce hematopoietic CSFs in cord blood may be important in HIV pathogenesis.     

Outbreak of rubella among cadets in an academy

Background: Rubella is traditionally considered a childhood disease, but has the potential to cause outbreaks in closed community of young adults. The present paper describes one such outbreak in a military training establishment.     

Management of Nucleus and IOL Drop

Background

Thirty six cases of lenticular nucleus drop following phacoemulsification and 43 cases of posterior dislocation of intraocular lens (IOL) inclusive of two paediatric cases were managed by a modified vitrectomy procedure without using perfluorocarbon liquid (PFCL).

Methods

In these cases the incision was placed inferotemporally at pars plana. The limbal sites of the earlier cataract surgery were utilised as the other two ports. In either case adequate vitrectomy was performed first. In cases of nuclear drop, the nucleus was impaled (speared) with a micro vitreo retinal blade and brought into the anterior chamber from where it was delivered out. In cases of IOL drop the same was picked up by an intra-vitreal forceps.

Result

Of the 77 adult cases treated 57 (74%) of the eyes had a visual recovery of 6/18 or more.

Conclusion

Prompt surgical management in cases of nuclear drop or posterior dislocation of IOL yields good results.Key Words: Phaco-emulsification, Intraocular lens drop, Nucleus drop, Vitrectomy     

Nodding syndrome: origins and natural history of a longstanding epileptic disorder in sub-Saharan Africa

Background

Repetitive involuntary head nodding was first reported in the 1960s in the Wapogoro tribe of Tanzania.

Objectives

We describe the natural history of head nodding in the Wapogoro tribe, with special reference to the earliest reported dates of onset.

Methods

We analyzed clinical data from 150 historical patients seen between 1960 and 1971.

Results

Head nodding with or without grand mal convulsions was present in 33/150 (∼20%) cases, was mostly familial and equally distributed by gender. Age at onset of head nodding ranged from 2–22 years (mean: ∼10 years) in the period 1934–1962. Head nodding preceded onset of grand mal convulsions by up to 12 months, and motor and psychomotor deficits indicative of brain damage developed with time. Fourteen of the 33 cases died at 13–39 years of age (mean: ∼20 years) while nineteen aged 16–28 years (mean: ∼16 years) were still alive.

Conclusion

Historical accounts of head nodding (amesinzia kichwa, Swahili) among the Wapogoro tribe fit the August 2012 World Health Organization (WHO) case definition of probable Nodding Syndrome. Reported to have existed in this population for at least 80 years, Nodding Syndrome is a progressive seizure disorder that leads to generalized convulsions (kifafa), brain damage and death.