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Of note, on the day of follow-up, he was on day 41 of the 45-day course of ATRA-induction therapy and had already completed idarubicin induction therapy. The macula of the left eye had preretinal hemorrhage over the fovea and extending inferonasally toward the inferotemporal arcades.
Optical coherence topography demonstrated marked thickening of the peripapillary retinal nerve fiber layer OU (Figure 3).
Egress of HSV-1 from Vero cells was examined initially with electron microscopy of thin-sectioned specimens. Further experiments were carried out with TIRF microscopy.TIRF was considered to be particularly appropriate for studying HSV-1 egress as it allows one to look specifically at the adherent surface of the infected cell, the site where the electron microscopic studies (described above) indicate much of the virus egress takes place.
Analysis by TIRF microscopy revealed that progeny HSV-1 virions clustered at specific sites along the adherent surface of the cell (Fig. At 4 hours post infection, Vero cells infected at an MOI of 10 showed neither glycoprotein staining nor HSV-K26-GFP virus signal (Fig. The GFP-labeled HSV-1 strain was used to examine the relationship of virus egress sites to the location of cytoskeletal structures. After infection, the distribution of all three cytoskeletal elements chaned significantly (see the center panels of Figs. All-trans retinoic acid (ATRA) induced intracranial hypertension in a patient with acute promyelocytic leukemia.
The virus-containing vesicle then traffics to the plasma membrane where it fuses, exposing a mature virion.
Monolayer cultures of Vero cells were infected with HSV-1 at an MOI of 10, and 12 hours post infection the cells were fixed and processed for electron microscopy. 2: HSV-1 glycoprotein enrichment at egress sites on the adherent surface of infected cells. 3: TIRF micrographs showing formation of glycoprotein patch sites are uncoupled from virus egress. 4: TIRF images of Vero cells infected for 12 hrs with GFP-labeled HSV-1 and then stained for microtubules (antibody stain), actin filaments (Phalloidin stain) and focal adhesions (vinculin-specific antibody stain). 6: TIRF micrographs showing egress site reformation after actin depolymerization-induced disruption.
7: Effect of gE and gE cytoplasmic tail deletions on patch formation and progeny virion trafficking. Pseudotumor cerebri induced by all-trans retinoic acid treatment of acute promyelocytic leukemia. Cerebrospinal fluid pressure in normal obese subjects and patients with pseudotumor cerebri. Maintained all-trans retinoic acid therapy in a patient with pseudotumour cerebri despite aggravated symptoms. Proof of differentiative mode of action of all-trans retinoic acid in acute promyelocytic leukemia using X-linked clonal analysis. Intracranial hypertension secondary to all-trans retinoic acid treatment for leukemia: diagnosis and management.
Pseudotumour cerebri in acute promyelocytic leukemia: improvement despite continued ATRA therapy. Treatment with all-trans retinoic acid and anthracycline monochemotherapy for children with acute promyelocytic leukemia: a multicenter study by the PETHEMA Group.


Management of acute promyelocytic leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet.
All-trans-retinoic acid (ATRA) responsive skin relapses of acute promyelocytic leukaemia followed by ATRA-induced pseudotumour cerebri.
GIMEMA-AIEOPAIDA protocol for the treatment of newly diagnosed acute promyelocytic leukemia (APL) in children. All-trans-retinoic acid and pseudotumor cerebri in a young adult with acute promyelocytic leukemia: a possible disease association. Retinol-binding protein and retinol analysis in cerebrospinal fluid and serum of patients with and without idiopathic intracranial hypertension. Pseudotumor cerebri caused by all-trans-retinoic acid treatment for acute promyelocytic leukemia. Micrographs showed that the majority of progeny virions were found at specific areas on the cell surface, rather than in a randomly dispersed pattern (see Figs. At 6 hpi small glycoprotein patches were detectable, although virions were rarely seen associated with them (Fig. These were stained, respectively, with an antibody specific for tubulin, Phalloidin and antibody specific for vinculin. Microtubules and actin filaments were disrupted with fibers no longer recognizable in most locations in the cell.
GFP-HSV-1-infected Vero cells at 11.5 hpi (A) were treated with cytochalasin B for 30 minutes (B). Exit is suggested to begin when virus-encoded glycoproteins accumulate at sites of the cell membrane where the cell is attached to the cell substrate or to another cell. It was expected that study of this adherent cell type would provide information about the role of cell-cell and cell-substrate contacts in HSV-1 egress when the effects of cell polarization are not present.
Note that the majority of virions are released in pockets along the adherent surface of the cell (arrowheads) and at cell-cell contact points (arrows).
TIRF studies added the observation that HSV-1 egress sites were enriched in virus membrane glycoproteins. Note that GFP-labeled virions were found to cluster at specific sites along the cell surface and glycosylated proteins accumulate at the same sites.
Focal adhesions were fewer in number, but not otherwise altered in appearance compared to uninfected cells (Fig. Infected monolayer Vero cells were examined by electron, confocal and total internal reflectance fluorescence microscopy. Virus-containing regions of the cell surface were located at sites of cell-cell contact and at sites along the adherent surface of the cell. Panel B shows an enlargement of the left arrowhead in A; panel C is an enlargement of the right. These were visualized by staining with wheat germ agglutinin (WGA) or with antibodies specific for individual virus glycoproteins (Fig.
By 8 hpi glycoprotein patches were more widespread and low levels of virus were consistently seen associated with the patches (Fig. Arrival of virus glycoproteins displaces cytoskeletal elements from the nascent exit sites.
Replication of Herpes Simplex Virus: Egress of Progeny Virus at Specialized Cell Membrane Sites.


Our observations revealed that HSV-1 was released at specific pocket-like areas of the plasma membrane that were found along the substrate-adherent surface and at regions of cell-cell contact.
Counts showed there were approximately three-fold more virions at adherent locations than on the non-adherent upper cell surface.
In all three cases, virus egress sites were found where cytoskeletal structures were absent.
Note that patches in the 4-12 hpi treatment sample are smaller with fewer virions compared to control. Deposition of virus glycoproteins and removal of cytoskeletal proteins is followed by attachment of virus-containing vesicles to the same sites. The studies also probed the role of virus glycoproteins and cytoskeletal structures such as microtubules and actin in exit of progeny HSV-1 virions. At both substrate-adherent and cell-cell exit sites, additional membrane was present allowing a curvature in the membrane and creation of a pocket-like structure (Figs. Note that, unlike infected cells, the cell membrane is closely apposed to the adherent surface. No comparable staining was observed when similar staining was done with uninfected cells (see Fig. Outline of cell was determined by increasing the brightness of the image until cell edge was visible. As expected, TIRF images of uninfected cells showed highly ordered arrays of microtubules and actin filaments (Fig. Virus-containing vesicles may be directed to exit sites by the presence of virus glycoproteins. In all cases the green-colored virion patches do not overlap with red cytoskeletal structures.
Infected cells were harvested at 10 hpi and titre was determined by limiting dilution plaque assay. Finally, there is a fusion event between the virus-containing vesicle membrane and the cytoplasmic membrane of the cell. Staining by both methods revealed that HSV-1 release sites were much more strongly stained than the surrounding cell membrane (compare Figs 2A and 2E).
By 6 hpi glycoprotein patches are beginning to form (arrow), but virus still is not evident.
It is concluded that virus egress sites are distinct from the sites of organized microtubules, actin filaments and focal adhesions. Note that gE deletions had little effect on the production of progeny virus titre in spite of the observation that the number of virions on the adherent surface was increased.
At 8 hpi there is pronounced glycoprotein staining on the cell surface and virions are beginning to accumulate in these areas. Although many virions were observed exterior to the plasma membrane in infected cells, none were seen near the interior side of the membrane (Figs.



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