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These type I IFNs are encoded by at least 14 IFN\u03b1 genes and a single IFN\u03b2 gene. We showed that the absence of one of the IFN\u03b1 genes (IFN\u03b12A\n                      <jats:sup>-\/-<\/jats:sup>\n                      ) affected latency levels in herpes simplex virus type 1 (HSV-1) ocularly infected mice but not in infected control mice, and the absence of IFN\u03b12A did not affect viral reactivation in ocularly infected mice. Since the role of IFN\u03b2 in HSV-1 latency reactivation and the potential effect of latency-associated transcript (LAT) on IFN\u03b2 activity is not known, we ocularly infected IFN\u03b2\n                      <jats:sup>-\/-<\/jats:sup>\n                      mice with different doses of LAT-plus [LAT(+)] and LAT-minus [LAT(-)] viruses. Wild-type (WT) control mice and IFN\u03b2\n                      <jats:sup>-\/-<\/jats:sup>\n                      mice were infected similarly. Virus titers in the eye, viral and cellular transcripts in the eye and trigeminal ganglia (TG) of infected mice on days 3 and 5 post-infection, eye disease, survival, latency-reactivation levels, and T cell exhaustion were measured in latently infected mice. Virus replication and viral and cellular transcripts in the eye of infected IFN\u03b2\n                      <jats:sup>-\/-<\/jats:sup>\n                      mice were similar to those in WT mice, while eye disease and survival in IFN\u03b2\n                      <jats:sup>-\/-<\/jats:sup>\n                      mice differed significantly from WT mice. WT mice infected with LAT(-) virus showed reduced latency, slower reactivation, and less T cell exhaustion than mice infected with LAT(+) virus. However, using different doses of each virus, latency levels, time of reactivation, and T cell exhaustion were similar between LAT(+) and LAT(-) viruses. These results suggest that the absence of IFN\u03b2 expression compensates for the function of LAT with regard to levels of latency, T cell exhaustion, and reactivation but does not affect viral and cellular transcripts during primary infection.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Interferon \u03b2 (IFN\u03b2) is a type I interferon that plays an important role in controlling primary herpes simplex virus type 1 (HSV-1) infection. To evaluate the importance of IFN\u03b2 on HSV-1 latency reactivation and its relationship to LAT, we infected IFN\u03b2\n                        <jats:sup>-\/-<\/jats:sup>\n                        mice with LAT(+) and LAT(-) viruses. In the absence of IFN\u03b2, latency levels in mice infected with LAT(-) virus were similar to those of mice infected with LAT(+) virus. The absence of IFN\u03b2 also reduced the time of reactivation in mice infected with LAT(-) virus to that of LAT(+) virus. Our results show a strong correlation between the functions of LAT and IFN\u03b2 during latent but not primary stages of HSV-1 infection.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.00374-25","type":"journal-article","created":{"date-parts":[[2025,5,12]],"date-time":"2025-05-12T09:00:33Z","timestamp":1747040433000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["IFN\u03b2 absence compensates for LAT functions in latency reactivation and T cell exhaustion"],"prefix":"10.1128","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7764-0581","authenticated-orcid":false,"given":"Shaohui","family":"Wang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02pammg90","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of 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