Fan deltas are excellent recorders of fan‐building processes because of their high sedimentation rate, particularly in tectonically active settings. Although previous research focuses mainly on allogenic controls, there is clear evidence for autogenically produced storage and release of sediment by flume and numerical modelling that demands further definition of characteristics and significance of autogenically forced facies and stratigraphy. Analogue experiments were performed on fan deltas with constant extrinsic variables (discharge, sediment supply, sea‐level and basin relief) to demonstrate that fan‐delta evolution consists of prominent cyclic alternations of channellized flow and sheet flow. The channellized flow is initiated by slope‐induced scouring and subsequent headward erosion to form a channel that connected with the valley, while the removed sediment is deposited in a rapidly prograding delta lobe. The resulting decrease in channel gradient causes a reduction in flow strength, mouth‐bar formation, flow bifurcation and progressive backfilling of the channel. In the final stage of channel filling, sheet flow coexists for a while with channellized flow (semi‐confined flow), although in cycle 1 this phase of semi‐confined flow was absent. Subsequent autocyclic incisions are very similar in morphology and gradient. However, they erode deeper into the delta plain and, as a result, take more time to backfill. The duration of the semi‐confined flow increases with each subsequent cycle. During the period of sheet flow, the delta plain aggrades up to the ‘critical’ gradient required for the initiation of autocyclic incision. This critical gradient is dependent on the sediment transport capacity, defined by the input conditions. These autogenic cycles of erosion and aggradation confirm earlier findings that storage and release of sediment and associated slope variation play an important role in fan‐delta evolution. The erosional surfaces produced by the autocyclic incisions are well‐preserved by the backfilling process in the deposits of the fan deltas. These erosional surfaces can easily be misinterpreted as climate, sea‐level or tectonically produced bounding surfaces.

Respiratory syncytial virus (RSV) is a major cause of severe lower respiratory tract infections in children, the elderly, and immune-compromised individuals. CD4 and CD8 T cells play a crucial role in the elimination of RSV from the infected lung, but T cell memory is not sufficient to completely prevent reinfections. The nature of the adaptive immune response depends on innate immune reactions initiated after interaction of invading pathogens with host APCs. For respiratory pathogens myeloid dendritic cell (DC) precursors that are located underneath the epithelial cell layer lining the airways may play a crucial role in primary activation of T cells and regulating their functional potential. In this study, we investigated the role of human monocyte-derived DC in RSV infection. We showed that monocyte-derived DC can be productively infected, which results in maturation of the DC judged by the up-regulation of CD80, CD83, CD86, and HLA class II molecules. However, RSV infection of DC caused impaired CD4 T cell activation characterized by a lower T cell proliferation and ablation of cytokine production in activated T cells. The suppressive effect was caused by an as yet unidentified soluble factor produced by RSV-infected DC.

A protective role for CD8+ T cells during viral infections is generally accepted, but little is known about how CD8+ T cell responses develop during primary infections in infants, their efficacy, and how memory is established after viral clearance. We studied CD8+ T cell responses in bronchoalveolar lavage (BAL) samples and blood of infants with a severe primary respiratory syncytial virus (RSV) infection. RSV-specific CD8+ T cells with an activated effector cell phenotype: CD27+CD28+CD45RO+CCR7−CD38+HLA-DR+Granzyme B+CD127− could be identified in BAL and blood. A high proportion of these CD8+ T cells proliferated and functionally responded upon in vitro stimulation with RSV Ag. Thus, despite the very young age of the patients, a robust systemic virus-specific CD8+ T cell response was elicited against a localized respiratory infection. RSV-specific T cell numbers as well as the total number of activated effector type CD8+ T cells peaked in blood around day 9–12 after the onset of primary symptoms, i.e., at the time of recovery. The lack of a correlation between RSV-specific T cell numbers and parameters of disease severity make a prominent role in immune pathology unlikely, in contrast the T cells might be involved in the recovery process.