Influenza viruses rarely cause acute encephalopathy. Post-influenza1 encephalitis, which occurs a few weeks after recovery from influenza is thought to be an autoimmune process associated with demyelination and vasculopathy. It has been suggested that Economo lethargic encephalitis followed by postencephalitic Parkinsonism was associated with the influenza A epidemic of 1918 (Spanish flu). The incidence of Reye's syndrome has markedly decreased due to the avoidance of salicylates in the treatment of influenza or varicella. One inactivated flu vaccine is thought to have caused Guillain Barre syndrome due to molecular mimicry between viral protein and myelin, which triggered autoimmune responses. The persistence of influenza virus genes in neural cells as one of the causes of chronic degenerative diseases of the central nervous system by inducing apoptosis of the host cells is yet to be proven.

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These results suggest that influenza viruses infect and probably persist in the gastric mucosa under conditions of acid suppression.

By growing VERO cells infected with 5 PFU/cell of influenza virus B/Lee/40, a latently infected culture was readily established (L/V cells). The cells continued to multiply stably, excreting a small amount of virus in the beginning, which sharply declined according to cell division to undetectable level by day 9. However, nucleotide sequences for all the 8 genes of B/Lee/40 as well as their mRNAs were amplified from L/V cells on day 50 or later by RT-PCR. Moreover, from the 95-day-old L/V cells, a persisting NP gene of B/Lee/40 was rescued into infectious virus particles upon superinfection with homotypic influenza virus B/Yamagata/1/73.

The reverse transcription polymerase chain reaction (RT-PCR) was performed to detect genes of RNA viruses in the freshly biopsied gastric mucosa of seven patients with low gastric acidity. Although nucleoprotein genes of Sendai virus and hemmaglutinin genes of influenza virus A were not detected, nucleoprotein genes of influenza virus B were detected in samples from three of the seven patients. The first patient had had antrectomy and vagotomy for gastric ulcer, the second patient was receiving a histamine type 2 receptor blocker for gastritis, and the third patient was receiving a proton pump inhibitor for gastric ulcer. Virus isolation from gastric mucosa and from gargles was negative for all seven patients. These findings suggest that genes of influenza viruses may exist in the gastric mucosa of patients with low gastric acidity.

When MDCK cells in a semiconfluent monolayer were infected with 5 p.f.u. per cell of influenza virus A/PR/8/34 (H1N1), a majority of the cells continued to grow stably upon subsequent cultivation with a growth medium containing 50 % foetal calf serum. While growing, the cells spontaneously excreted virus, the amount of which declined gradually as the passage number of the cells increased. The extent of virus shedding was significantly increased when the cells were subsequently maintained in a medium containing 0n2 % bovine serum albumin. Within the cells, viral messenger RNAs for all eight genes of A/PR/8 were demonstrated by PCR indicating that endogenous viral genes were constitutively transcribed. However, viral proteins as well as viral genes were not demonstrable by radioimmunoprecipitation or ribonuclease protection assays, respectively. (De & Nayak, 1980 ;Frielle et al., 1984 ;Goshima & Maeno, 1989 ;Marschall et al., 1993) or long-term persistence of viral genomes in susceptible host cells (Cane et al., 1987 ;Cane & Dimmock, 1990 ;Urabe et al., 1992 Urabe et al., , 1993. In addition, Urabe et al. (1994) presented evidence that persisting viral genes were self-amplified during their persistence within cells. These results clearly indicate that two quite heterogeneous genetic systems, namely that of influenza virus and that of host cells, are not mutually exclusive, and that the genome of even a highly cytolytic virus such as influenza virus can remain in the host cell for a considerable time under certain conditions. Defective interfering (DI) virus is reportedly involved in the establishment of persistent infection with influenza virus (De & Nayak, 1980 ;Frielle et al., 1984). Several investigators have described persistent infection with influenza virusWe infected a semiconfluent monolayer of 5i10& MDCK cells with 5 p.f.u. per cell of plaque-purified wild-type influenza Author for correspondence : Kiyotake Tobita.Fax j81 285 44 4981. e-mail tobikiyo!jichi.ac.jp virus A\PR\8\34, free from a significant amount of DI virus. After 30 min at room temperature, Eagle's minimum essential medium (MEM) supplemented with 0n2 % bovine serum albumin (BSA) (MEMjBSA) was added, and the cells were incubated for 1 h at 34 mC. The cells were then washed five times with PBS, and incubated with MEM supplemented with 50 % foetal calf serum (FCS) (MEMj50 % FCS) at 34 mC. A majority of the cells continued to grow stably without any appreciable crisis. For stable growth of the infected cells, 50 % FCS was required. Less concentrated FCS in the growth medium resulted in eventual destruction of the culture.At appropriate times post-infection (p.i.), the culture medium was removed for infectivity assay. The cells were then washed five times with PBS and re-fed with fresh MEMj50 % FCS, or subcultured.

This study was undertaken to identify characteristics of residents who left their training program before the end of the program. A survey was sent to 248 Program Directors in the United States, after institutional review. Anonymous responses were received from 27 (11%) programs. Data was received on 166 residents, including 111 males and 55 females. The group included 146 categorical residents and 20 preliminary residents. Of these, 60 residents left in the middle of the year and 105 left at the end of the year. Of the 164 residents for whom data was reported, 30 (21%) used counseling services. Of 110 residents who left before 2004, 54 (49%) left to choose another specialty. In 2004, of 25 residents who left, 13 (52%, P > 0.05) pursued training in another specialty, and in 2005 of 31 residents who left, 23 (74%, P < 0.025) chose another specialty. Significantly more residents who started a career in surgery after 2004 left to train in another specialty. This may be due to implementation of work hour restrictions in 2003 leading residents to enter surgery who would not have done so previously. Strategies for better retention of matched residents are necessary to reverse this worrisome trend.