Mortalities of cultured shrimp, Penaeus vannamei (Boone), induced by white spot syndrome virus (WSSV) have occurred in Ecuador since May 1999. Three epidemiological surveys in Ecuadorian farms were carried out and showed an apparent association between lower temperature and increased mortality rates in commercial ponds. Infected animals showed a reddish discolouration and lethargy and occasionally, white spots in the exoskeleton. Histopathological studies revealed that infected cells presented nuclear hypertrophy with eosinophilic to basophilic inclusions. In some cases, two other pathologies were observed: (a) lymphoid organ spheroids and (b) cells with pyknotic and karyorrhectic nuclei in the lymphoid organ, haematopoietic tissue, connective tissue, heart and antennal gland. Occasionally pyknotic cells were encapsulated without apparent injury to the adjacent tissue and without melanization. Transmission electron microscopy showed the presence of WSSV particles in the cytoplasm of cells with pyknotic nuclei in the stomach hypodermis. Viral structure and morphogenesis agreed with previous descriptions by other authors in WSSV-infected shrimp. Occasionally, two nucleocapsids within one envelope were present amongst single enveloped nucleocapsids. A long rod-shaped structure that could reach 2.4 lm in length was present in the nuclei of some infected cells.

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The hemagglutination (HA) and receptor destroying enzyme (RDE) activities of a newly isolated mouse enteric coronavirus (designated as DVIM) are described. DVIM agglutinates mouse or rat red blood cells (RBC) at 4 degrees C. At 37 degrees C the agglutination was rapidly reversed. The optimal pH for HA and for RDE activities using mouse red cells were shown to be 6.5 and 7.3 respectively. Hemagglutination by DVIM was not inhibited by pretreatment of RBCs with Vibrio cholerae filtrate or by pretreatment with Influenza-A neuraminidase. Therefore, the DVIM receptors on RBCs differ from the receptors of Influenza-A, and the RDE activity of DVIM acts specifically on this receptor. In addition, an analysis of the DVIM polypeptides showed that the virions contain five major, VP1 (M.W. 139,000), VP2 (68,000), VP3 (53,000), VP4 (38,000), VP5 (22,000) and two minor, VP1a (110,000), VP1b (100,000) polypeptides. VP1 and VP1b were digested by bromelain, suggesting that they constitute the surface glycoproteins.

SummaryBiological and morphological properties of ~ virus, isolated from the intestine of infant mice with clinical signs of diarrhea and designated as diarrhea virus of infant mice (DVIM), were examined. The first infective virus was detected on the cells 4 hours post infection, followed by rapid release of the virus into the culture fluids. Virus-induced syncytia in BALB/c-3T3 cell cultures caused hemadsorption at 4 ° C and viral antigens were shown to be located in the cytoplasm of the syncy~ia by immunofluorescent techniques. By scanning electron-microscopy, budding virus-like particles were detected on the surface of virus-induced syncytia. Morphologically the virus was shown to be enveloped and approximately 100 nm in diameter. Two types of projections were demonstrated, one type of projection was club-shaped, 20 nm in length and the other type was small, granular, 5 nm in length. The latter type of projection might be the basal part of the clubshaped type and related to the hemagglutinating activity.

Larvae and post-larvae of Penaeus vannamei (Boone) were submitted to primary challenge with infectious hypodermal and haematopoietic necrosis virus (IHHNV) or formalin-inactivated white spot syndrome virus (WSSV). Survival rate and viral load were evaluated after secondary per os challenge with WSSV at post-larval stage 45 (PL45). Only shrimp treated with inactivated WSSV at PL35 or with IHHNV infection at nauplius 5, zoea 1 and PL22 were alive (4.7% and 4%, respectively) at 10 days post-infection (p.i.). Moreover, at 9 days p.i. there was 100% mortality in all remaining treatments, while there was 94% mortality in shrimp treated with inactivated WSSV at PL35 and 95% mortality in shrimp previously treated with IHHNV at N5, Z1 and PL22. Based on viral genome copy quantification by real-time PCR, surviving shrimp previously challenged with IHHNV at PL22 contained the lowest load of WSSV (0-1x10(3) copies microg-1 of DNA). In addition, surviving shrimp previously exposed to inactivated WSSV at PL35 also contained few WSSV (0-2x10(3) copies microg-1 of DNA). Consequently, pre-exposure to either IHHNV or inactivated WSSV resulted in slower WSSV replication and delayed mortality. This evidence suggests a protective role of IHHNV as an interfering virus, while protection obtained by inactivated WSSV might result from non-specific antiviral immune response.