Abstract: A method for the treatment for hepatitis delta infection in a host, that includes administering an effective amount of a nucleoside or a nucleoside analog that suppresses the expression of the hepatitis B surface or preS1 antigen in the host 100-fold or more relative to pretreatment values in vivo; or to not more than 1 microgram per milliliter in vivo. In a preferred embodiment, the nucleoside is L-FMAU, or a pharmaceutically acceptable salt or prodrug thereof.

Abstract: A method for the treatment for hepatitis delta infection in a host, that includes administering an effective amount of a nucleoside or a nucleoside analog that suppresses the expression of the hepatitis B surface or preS1 antigen in the host 100-fold or more relative to pretreatment values in vivo; or to not more than 1 microgram per milliliter in vivo. In a preferred embodiment, the nucleoside is L-FMAU, or a pharmaceutically acceptable salt or prodrug thereof.

Abstract: A method for the treatment for hepatitis delta infection in a host, that includes administering an effective amount of a nucleoside or a nucleoside analog that suppresses the expression of the hepatitis B surface or preS1 antigen in the host 100-fold or more relative to pretreatment values in vivo; or to not more than 1 microgram per milliliter in vivo. In a preferred embodiment, the nucleoside is L-FMAU, or a pharmaceutically acceptable salt or prodrug thereof.

Abstract: Antisense oligonucleotides that hybridize to segments of the pres1, S, C, and &egr; regions of the hepatitis B virus (HBV) RNA pregenome inhibit replication of the virus. Pharmaceutical compositions which contain these oligonucleotides as the active ingredients are effective against HBV infection.

Abstract: A method for the treatment for hepatitis delta infection in a host, that includes administering an effective amount of a nucleoside or a nucleoside analog that suppresses the expression of the hepatitis B surface or preS1 antigen in the host 100-fold or more relative to pretreatment values in vivo; or to not more than 1 microgram per milliliter in vivo. In a preferred embodiment, the nucleoside is L-FMAU, or a pharmaceutically acceptable salt or prodrug thereof.

Abstract: Antisense oligonucleotides that hybridize to segments of the preS1, S, C, and .epsilon. regions of the hepatitis B virus (HBV) RNA pregenome inhibit replication of the virus. Pharmaceutical compositions which contain these oligonucleotides as the active ingredients are effective against HBV infection.

Abstract: Interferon introduced parenterally in a human host or stimulated by an inducer (PICLC) for a period of greater than 21 days results in a major decrease in all markers of infectivity, such as DNA polymerase, and such markers remain at a depressed level during the period of treatment. Where PICLC is utilized to induce interferon in the host, a serum level of 50 units per milliliter or higher is necessary for effective clinical treatment and 17 .times. 10.sup.4 - 6.0 .times. 10.sup.3 U/kg/day is an effective dose for exogenous interferon. Especially long-term treatment with exogenous interferon of greater than 21 days and up to 14 months results in clinical improvement for chronic hepatitis B virus (HBV) infection and this long-term treatment has resulted in sustained improvement even after cessation of treatment as well as resulting in a decrease in infectivity risk to others in close proximity to the infected human host. Such clinical improvement is marked by normalization of liver histology.