Herpes simplex keratitis (HSK) is one of the most challenging ocular diseases faced by ophthalmologists, and proper diagnosis and treatment are important for its prognosis. HSK has multiple clinical types, and due to the complexity and inconsistency of the previous classification, Holland et al. proposed a new classification in 1999, which divided it into four categories based on anatomical and pathophysiological features: infectious keratitis, stromal keratitis, neurotrophic corneal ulcer, and endothelial keratitis. The proposed new classification by Holland et al. has greatly improved the quality of clinical diagnosis and treatment of HSK. However, there are still two misconceptions in the diagnosis and treatment of HSK: 1. The disease is thought to be caused by a single viral replication disruption factor, and the use of antiviral drugs is the only measure to treat all types of HSK, and even “preventive drugs” for fear of recurrence. 2, that hormones are absolutely contraindicated in the treatment of all types of HSK, even in immune keratoconjunctivitis and endotheliitis, resulting in delayed disease and irreversible endothelial damage, so that some patients who could recover quickly with hormone therapy eventually had to resort to penetrating corneal transplantation. These two misconceptions tend to complicate the above four basic types of herpes simplex virus keratitis, resulting in two specific types of herpes simplex virus keratitis that are easily confused by clinicians and relatively difficult to treat, as discussed in this article. In clinical practice, we sometimes encounter patients with superficial lesions such as infected corneal epithelium or neurotrophic ulcers combined with deeper lesions such as immune stromal keratitis or endothelial keratitis that do not belong to any of the Holland classifications, and we call the presence of two or more different parts of the cornea involved mixed herpes simplex virus keratitis. . The mechanism of corneal epithelial and superficial stromal ulcers combined with corneal immune stromal inflammation is the involvement of both destructive and immune factors caused by viral replication. However, due to the presence of immune stromal inflammation or endothelial inflammation, antiviral therapy alone often fails to rapidly control the disease and even results in irreversible endothelial loss, eventually requiring penetrating corneal transplantation. Our experience is to apply corticosteroids appropriately in the context of antiviral therapy. Corticosteroids suppress tissue immune response, reduce infiltrative edema and inflammatory damage to tissue, reduce scarring and neovascularization, promote healing of keratitis, and improve visual acuity. In principle, adequate local and systemic antiviral therapy is administered first, while systemic hormones can be applied for several days. After healing of epithelial and superficial stromal lesions, the application of local hormonal eye drops is started and gradually reduced to a minimum concentration and minimum number of times, which can be discontinued only when the inflammation subsides and lasts for a period of time to prevent recurrence. The pathogenesis of neurotrophic ulcers combined with immune keratoconjunctivitis and/or endothelial keratitis is due to a variety of factors, including basement membrane damage, tear dysfunction and neurotrophic disorders caused by viral nerve damage, and drug toxicity caused by long-term topical drug use, combined with immune inflammation of the corneal stroma or endothelium. Most of the anterior elastic layer disappears and is replaced by connective tissue or neovascularization. The epithelial basal cells are swollen and loosely attached to the underlying deeper tissue. This is the pathological basis for the formation of neurotrophic corneal ulcers. On this basis, drug toxicity caused by the abuse of antiviral drugs, basement membrane damage and epithelial defects caused by inappropriate debridement therapy and decongestive treatment, and failure to give timely and adequate hormonal treatment are the main causes of this type. The initial ocular infection of HSK is often manifested as conjunctivitis, corneal epithelial defects, etc. Corneal stromal involvement is rare, and most of them have no prognosis, which is the reason why many adult patients complain that they have never had HSK, and also the reason why the physicians ignore HSK after anterior segment surgery. Ophthalmic surgery is also a causative factor, which is less commonly reported in clinical practice. With the increasing number of cataract surgeries and refractive surgeries, post-operative herpes moniliformis keratitis is becoming more common. The pathogenesis may be related to the longer time and higher concentration of postoperative hormone application, especially in some patients with corneal edema requiring hormone therapy after surgery, which is more likely to lead to potential viral recurrence and spread, while surgical trauma itself, advanced age and decreased resistance are also important predisposing factors. Patients with typical symptoms of ocular pain, photophobia and tearing, vision loss and signs of punctate or dendritic infiltration of the corneal epithelium after anterior segment surgery can be cured rapidly with a good prognosis if given topical Lycopodium gel or oral acyclovir tablets at an early stage. If the performance is atypical, such as keratoconjunctivitis and endotheliitis, easily misdiagnosed as bacterial keratitis or other types of keratitis such as corneal endothelial loss, treatment is given a large number of antibiotic eye drops and other eye drops, on the basis of viral keratitis there is a serious corneal drug toxicity reaction, and even some patients have the manifestation of dry eye, making treatment more difficult.